RapamycinFungusV1, Main, Exploration, bibRecord, 000870

Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.

Identifieur interne : 000870 ( Main/Exploration ); précédent : 000869; suivant : 000871

Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.

Auteurs : Ao Bian [République populaire de Chine, États-Unis] ; Mingjun Shi [États-Unis] ; Brianna Flores [États-Unis] ; Nancy Gillings [États-Unis] ; Peng Li [République populaire de Chine] ; Shirley Xiao Yan [États-Unis] ; Beth Levine [États-Unis] ; Changying Xing [République populaire de Chine] ; Ming Chang Hu [États-Unis]

Source :

PloS one [ 1932-6203 ] ; 2017.

RBID : pubmed:28886014

Descripteurs français

KwdFr :
- Animaux (MeSH), Atteinte rénale aigüe (anatomopathologie), Atteinte rénale aigüe (étiologie), Autophagie (effets des médicaments et des substances chimiques), Autophagie (génétique), Bécline-1 (métabolisme), Cellules épithéliales (métabolisme), Expression des gènes (MeSH), Humains (MeSH), Indice de gravité de la maladie (MeSH), Lapins (MeSH), Liaison aux protéines (MeSH), Lésion d'ischémie-reperfusion (anatomopathologie), Lésion d'ischémie-reperfusion (complications), Lésion d'ischémie-reperfusion (génétique), Modèles animaux de maladie humaine (MeSH), Protéine C-réactive (génétique), Protéine C-réactive (métabolisme), Protéines proto-oncogènes c-bcl-2 (métabolisme), Sirolimus (pharmacologie), Souris (MeSH), Tubules rénaux (métabolisme).
MESH :
- anatomopathologie : Atteinte rénale aigüe, Lésion d'ischémie-reperfusion.
- effets des médicaments et des substances chimiques : Autophagie.
- génétique : Autophagie, Lésion d'ischémie-reperfusion, Protéine C-réactive.
- métabolisme : Bécline-1, Cellules épithéliales, Protéine C-réactive, Protéines proto-oncogènes c-bcl-2, Tubules rénaux.
- pharmacologie : Sirolimus.
- étiologie : Atteinte rénale aigüe.
- Animaux, Expression des gènes, Humains, Indice de gravité de la maladie, Lapins, Liaison aux protéines, Modèles animaux de maladie humaine, Souris.

English descriptors

KwdEn :
- Acute Kidney Injury (etiology), Acute Kidney Injury (pathology), Animals (MeSH), Autophagy (drug effects), Autophagy (genetics), Beclin-1 (metabolism), C-Reactive Protein (genetics), C-Reactive Protein (metabolism), Disease Models, Animal (MeSH), Epithelial Cells (metabolism), Gene Expression (MeSH), Humans (MeSH), Kidney Tubules (metabolism), Mice (MeSH), Protein Binding (MeSH), Proto-Oncogene Proteins c-bcl-2 (metabolism), Rabbits (MeSH), Reperfusion Injury (complications), Reperfusion Injury (genetics), Reperfusion Injury (pathology), Severity of Illness Index (MeSH), Sirolimus (pharmacology).
MESH :
- chemical , genetics : C-Reactive Protein.
- chemical , metabolism : Beclin-1, C-Reactive Protein, Proto-Oncogene Proteins c-bcl-2.
- complications : Reperfusion Injury.
- drug effects : Autophagy.
- etiology : Acute Kidney Injury.
- genetics : Autophagy, Reperfusion Injury.
- metabolism : Epithelial Cells, Kidney Tubules.
- pathology : Acute Kidney Injury, Reperfusion Injury.
- chemical , pharmacology : Sirolimus.
- Animals, Disease Models, Animal, Gene Expression, Humans, Mice, Protein Binding, Rabbits, Severity of Illness Index.

Abstract

C-reactive protein (CRP), was recently reported to be closely associated with poor renal function in patients with acute kidney injury (AKI), but whether CRP is pathogenic or a mere biomarker in AKI remains largely unclear. Impaired autophagy is known to exacerbate renal ischemia-reperfusion injury (IRI). We examined whether the pathogenic role of CRP in AKI is associated with reduction of autophagy. We mated transgenic rabbit CRP over-expressing mice (Tg-CRP) with two autophagy reporter mouse lines, Tg-GFP-LC3 mice (LC3) and Tg-RFP-GFP-LC3 mice (RG-LC3) respectively to generate Tg-CRP-GFP-LC3 mice (PLC3) and Tg-CRP-RFP-GFP-LC3 mice (PRG-LC3). AKI was induced by IRI. Compared with LC3 mice, PLC3 mice developed more severe kidney damage after IRI. Renal tubules were isolated from LC3 mice at baseline for primary culture. OKP cells were transiently transfected with GFP-LC3 plasmid. CRP addition exacerbated lactate dehydrogenase release from both cell types. Immunoblots showed lower LC-3 II/I ratios and higher levels of p62, markers of reduced autophagy flux, in the kidneys of PLC3 mice compared to LC3 mice after IRI, and in primary cultured renal tubules and OKP cells treated with CRP and H2O2 compared to H2O2 alone. Immunohistochemistry showed much fewer LC-3 punctae, and electron microscopy showed fewer autophagosomes in kidneys of PLC3 mice compared to LC3 mice after IRI. Similarly, CRP addition reduced GFP-LC3 punctae induced by H2O2 in primary cultured proximal tubules and in GFP-LC3 plasmid transfected OKP cells. Rapamycin, an autophagy inducer, rescued impaired autophagy and reduced renal injury in vivo. In summary, it was suggested that CRP be more than mere biomarker in AKI, and render the kidney more susceptible to ischemic/oxidative injury, which is associated with down-regulating autophagy flux.

DOI: 10.1371/journal.pone.0181848
PubMed: 28886014
PubMed Central: PMC5590740

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000736
to stream Main, to step Curation: 000736

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.</title>
<author><name sortKey="Bian, Ao" sort="Bian, Ao" uniqKey="Bian A" first="Ao" last="Bian">Ao Bian</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu</wicri:regionArea>
<wicri:noRegion>Jiangsu</wicri:noRegion>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Shi, Mingjun" sort="Shi, Mingjun" uniqKey="Shi M" first="Mingjun" last="Shi">Mingjun Shi</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Flores, Brianna" sort="Flores, Brianna" uniqKey="Flores B" first="Brianna" last="Flores">Brianna Flores</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gillings, Nancy" sort="Gillings, Nancy" uniqKey="Gillings N" first="Nancy" last="Gillings">Nancy Gillings</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Li, Peng" sort="Li, Peng" uniqKey="Li P" first="Peng" last="Li">Peng Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu</wicri:regionArea>
<wicri:noRegion>Jiangsu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yan, Shirley Xiao" sort="Yan, Shirley Xiao" uniqKey="Yan S" first="Shirley Xiao" last="Yan">Shirley Xiao Yan</name>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Xing, Changying" sort="Xing, Changying" uniqKey="Xing C" first="Changying" last="Xing">Changying Xing</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu</wicri:regionArea>
<wicri:noRegion>Jiangsu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Hu, Ming Chang" sort="Hu, Ming Chang" uniqKey="Hu M" first="Ming Chang" last="Hu">Ming Chang Hu</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2017">2017</date>
<idno type="RBID">pubmed:28886014</idno>
<idno type="pmid">28886014</idno>
<idno type="doi">10.1371/journal.pone.0181848</idno>
<idno type="pmc">PMC5590740</idno>
<idno type="wicri:Area/Main/Corpus">000736</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000736</idno>
<idno type="wicri:Area/Main/Curation">000736</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000736</idno>
<idno type="wicri:Area/Main/Exploration">000736</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.</title>
<author><name sortKey="Bian, Ao" sort="Bian, Ao" uniqKey="Bian A" first="Ao" last="Bian">Ao Bian</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu</wicri:regionArea>
<wicri:noRegion>Jiangsu</wicri:noRegion>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Shi, Mingjun" sort="Shi, Mingjun" uniqKey="Shi M" first="Mingjun" last="Shi">Mingjun Shi</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Flores, Brianna" sort="Flores, Brianna" uniqKey="Flores B" first="Brianna" last="Flores">Brianna Flores</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Gillings, Nancy" sort="Gillings, Nancy" uniqKey="Gillings N" first="Nancy" last="Gillings">Nancy Gillings</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Li, Peng" sort="Li, Peng" uniqKey="Li P" first="Peng" last="Li">Peng Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu</wicri:regionArea>
<wicri:noRegion>Jiangsu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Yan, Shirley Xiao" sort="Yan, Shirley Xiao" uniqKey="Yan S" first="Shirley Xiao" last="Yan">Shirley Xiao Yan</name>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Xing, Changying" sort="Xing, Changying" uniqKey="Xing C" first="Changying" last="Xing">Changying Xing</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu</wicri:regionArea>
<wicri:noRegion>Jiangsu</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Hu, Ming Chang" sort="Hu, Ming Chang" uniqKey="Hu M" first="Ming Chang" last="Hu">Ming Chang Hu</name>
<affiliation wicri:level="2"><nlm:affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">PloS one</title>
<idno type="eISSN">1932-6203</idno>
<imprint><date when="2017" type="published">2017</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Kidney Injury (etiology)</term>
<term>Acute Kidney Injury (pathology)</term>
<term>Animals (MeSH)</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy (genetics)</term>
<term>Beclin-1 (metabolism)</term>
<term>C-Reactive Protein (genetics)</term>
<term>C-Reactive Protein (metabolism)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Epithelial Cells (metabolism)</term>
<term>Gene Expression (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Kidney Tubules (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Protein Binding (MeSH)</term>
<term>Proto-Oncogene Proteins c-bcl-2 (metabolism)</term>
<term>Rabbits (MeSH)</term>
<term>Reperfusion Injury (complications)</term>
<term>Reperfusion Injury (genetics)</term>
<term>Reperfusion Injury (pathology)</term>
<term>Severity of Illness Index (MeSH)</term>
<term>Sirolimus (pharmacology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Atteinte rénale aigüe (anatomopathologie)</term>
<term>Atteinte rénale aigüe (étiologie)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Autophagie (génétique)</term>
<term>Bécline-1 (métabolisme)</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Expression des gènes (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Indice de gravité de la maladie (MeSH)</term>
<term>Lapins (MeSH)</term>
<term>Liaison aux protéines (MeSH)</term>
<term>Lésion d'ischémie-reperfusion (anatomopathologie)</term>
<term>Lésion d'ischémie-reperfusion (complications)</term>
<term>Lésion d'ischémie-reperfusion (génétique)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Protéine C-réactive (génétique)</term>
<term>Protéine C-réactive (métabolisme)</term>
<term>Protéines proto-oncogènes c-bcl-2 (métabolisme)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Tubules rénaux (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>C-Reactive Protein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term>
<term>C-Reactive Protein</term>
<term>Proto-Oncogene Proteins c-bcl-2</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Atteinte rénale aigüe</term>
<term>Lésion d'ischémie-reperfusion</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Reperfusion Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Acute Kidney Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term>
<term>Reperfusion Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Autophagie</term>
<term>Lésion d'ischémie-reperfusion</term>
<term>Protéine C-réactive</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term>
<term>Kidney Tubules</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term>
<term>Cellules épithéliales</term>
<term>Protéine C-réactive</term>
<term>Protéines proto-oncogènes c-bcl-2</term>
<term>Tubules rénaux</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Acute Kidney Injury</term>
<term>Reperfusion Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Atteinte rénale aigüe</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>Gene Expression</term>
<term>Humans</term>
<term>Mice</term>
<term>Protein Binding</term>
<term>Rabbits</term>
<term>Severity of Illness Index</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Expression des gènes</term>
<term>Humains</term>
<term>Indice de gravité de la maladie</term>
<term>Lapins</term>
<term>Liaison aux protéines</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">C-reactive protein (CRP), was recently reported to be closely associated with poor renal function in patients with acute kidney injury (AKI), but whether CRP is pathogenic or a mere biomarker in AKI remains largely unclear. Impaired autophagy is known to exacerbate renal ischemia-reperfusion injury (IRI). We examined whether the pathogenic role of CRP in AKI is associated with reduction of autophagy. We mated transgenic rabbit CRP over-expressing mice (Tg-CRP) with two autophagy reporter mouse lines, Tg-GFP-LC3 mice (LC3) and Tg-RFP-GFP-LC3 mice (RG-LC3) respectively to generate Tg-CRP-GFP-LC3 mice (PLC3) and Tg-CRP-RFP-GFP-LC3 mice (PRG-LC3). AKI was induced by IRI. Compared with LC3 mice, PLC3 mice developed more severe kidney damage after IRI. Renal tubules were isolated from LC3 mice at baseline for primary culture. OKP cells were transiently transfected with GFP-LC3 plasmid. CRP addition exacerbated lactate dehydrogenase release from both cell types. Immunoblots showed lower LC-3 II/I ratios and higher levels of p62, markers of reduced autophagy flux, in the kidneys of PLC3 mice compared to LC3 mice after IRI, and in primary cultured renal tubules and OKP cells treated with CRP and H2O2 compared to H2O2 alone. Immunohistochemistry showed much fewer LC-3 punctae, and electron microscopy showed fewer autophagosomes in kidneys of PLC3 mice compared to LC3 mice after IRI. Similarly, CRP addition reduced GFP-LC3 punctae induced by H2O2 in primary cultured proximal tubules and in GFP-LC3 plasmid transfected OKP cells. Rapamycin, an autophagy inducer, rescued impaired autophagy and reduced renal injury in vivo. In summary, it was suggested that CRP be more than mere biomarker in AKI, and render the kidney more susceptible to ischemic/oxidative injury, which is associated with down-regulating autophagy flux.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28886014</PMID>
<DateCompleted><Year>2017</Year>
<Month>10</Month>
<Day>18</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>12</Volume>
<Issue>9</Issue>
<PubDate><Year>2017</Year>
</PubDate>
</JournalIssue>
<Title>PloS one</Title>
<ISOAbbreviation>PLoS One</ISOAbbreviation>
</Journal>
<ArticleTitle>Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.</ArticleTitle>
<Pagination><MedlinePgn>e0181848</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0181848</ELocationID>
<Abstract><AbstractText>C-reactive protein (CRP), was recently reported to be closely associated with poor renal function in patients with acute kidney injury (AKI), but whether CRP is pathogenic or a mere biomarker in AKI remains largely unclear. Impaired autophagy is known to exacerbate renal ischemia-reperfusion injury (IRI). We examined whether the pathogenic role of CRP in AKI is associated with reduction of autophagy. We mated transgenic rabbit CRP over-expressing mice (Tg-CRP) with two autophagy reporter mouse lines, Tg-GFP-LC3 mice (LC3) and Tg-RFP-GFP-LC3 mice (RG-LC3) respectively to generate Tg-CRP-GFP-LC3 mice (PLC3) and Tg-CRP-RFP-GFP-LC3 mice (PRG-LC3). AKI was induced by IRI. Compared with LC3 mice, PLC3 mice developed more severe kidney damage after IRI. Renal tubules were isolated from LC3 mice at baseline for primary culture. OKP cells were transiently transfected with GFP-LC3 plasmid. CRP addition exacerbated lactate dehydrogenase release from both cell types. Immunoblots showed lower LC-3 II/I ratios and higher levels of p62, markers of reduced autophagy flux, in the kidneys of PLC3 mice compared to LC3 mice after IRI, and in primary cultured renal tubules and OKP cells treated with CRP and H2O2 compared to H2O2 alone. Immunohistochemistry showed much fewer LC-3 punctae, and electron microscopy showed fewer autophagosomes in kidneys of PLC3 mice compared to LC3 mice after IRI. Similarly, CRP addition reduced GFP-LC3 punctae induced by H2O2 in primary cultured proximal tubules and in GFP-LC3 plasmid transfected OKP cells. Rapamycin, an autophagy inducer, rescued impaired autophagy and reduced renal injury in vivo. In summary, it was suggested that CRP be more than mere biomarker in AKI, and render the kidney more susceptible to ischemic/oxidative injury, which is associated with down-regulating autophagy flux.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bian</LastName>
<ForeName>Ao</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shi</LastName>
<ForeName>Mingjun</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Flores</LastName>
<ForeName>Brianna</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gillings</LastName>
<ForeName>Nancy</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Peng</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Yan</LastName>
<ForeName>Shirley Xiao</ForeName>
<Initials>SX</Initials>
<AffiliationInfo><Affiliation>Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Levine</LastName>
<ForeName>Beth</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Departments of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Autophagy Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xing</LastName>
<ForeName>Changying</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Ming Chang</ForeName>
<Initials>MC</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-3235-8301</Identifier>
<AffiliationInfo><Affiliation>Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States of America.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 CA109618</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 DK092461</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>09</Month>
<Day>08</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>PLoS One</MedlineTA>
<NlmUniqueID>101285081</NlmUniqueID>
<ISSNLinking>1932-6203</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071186">Beclin-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D019253">Proto-Oncogene Proteins c-bcl-2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>9007-41-4</RegistryNumber>
<NameOfSubstance UI="D002097">C-Reactive Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber>
<NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D058186" MajorTopicYN="N">Acute Kidney Injury</DescriptorName>
<QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002097" MajorTopicYN="N">C-Reactive Protein</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015870" MajorTopicYN="Y">Gene Expression</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007684" MajorTopicYN="N">Kidney Tubules</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019253" MajorTopicYN="N">Proto-Oncogene Proteins c-bcl-2</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015427" MajorTopicYN="N">Reperfusion Injury</DescriptorName>
<QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year>
<Month>06</Month>
<Day>29</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>07</Month>
<Day>07</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2017</Year>
<Month>9</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2017</Year>
<Month>9</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2017</Year>
<Month>10</Month>
<Day>19</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>epublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">28886014</ArticleId>
<ArticleId IdType="doi">10.1371/journal.pone.0181848</ArticleId>
<ArticleId IdType="pii">PONE-D-16-24975</ArticleId>
<ArticleId IdType="pmc">PMC5590740</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>Kidney Int. 2004 Aug;66(2):500-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15253697</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2013 Sep;84(3):468-81</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23636173</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2004 Apr;65(4):1357-65</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15086475</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Crit Care Med. 2008 Apr;36(4 Suppl):S187-92</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18382192</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell. 2008 Jun 20;30(6):678-88</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18570871</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Pathol. 2012 Feb;180(2):517-25</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22265049</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2012 Mar;81(5):477-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22157656</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Methods Enzymol. 2009;452:13-23</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19200873</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2011 Jul;80(1):29-40</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21562469</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int Suppl (2011). 2012 Mar;2(1):19-36</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25018918</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13043-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12244213</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Exp Med. 1961 Dec 1;114:961-74</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14460901</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Gene. 1991 Dec 15;108(2):193-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">1660837</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2007 Apr;18(4):1292-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17314324</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2575-80</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9122237</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>FASEB J. 2010 Sep;24(9):3438-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20466874</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Arch Med Res. 2008 Apr;39(3):326-31</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18279706</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Circ Res. 2007 May 25;100(10):1452-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17446434</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2012 Dec;82(12):1250-3</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23203020</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Diabetes. 2013 Mar;62(3):721-31</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23069625</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Circulation. 2007 Feb 27;115(8):1020-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17283257</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Clin J Am Soc Nephrol. 2015 Aug 7;10(8):1324-31</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26195505</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Bone Miner Res. 2015 Dec;30(12 ):2249-61</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26077727</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Res. 2014 Jan;24(1):69-79</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24323045</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 2011 Mar;121(3):1026-43</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21339643</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2011 Sep;7(9):1085-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21606682</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Clin Sci (Lond). 2014 May;126(9):645-59</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24206243</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Physiol Renal Physiol. 2013 Jun 1;304(11):F1358-65</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23535585</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Heart. 2002 Mar;87(3):201-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11847151</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO J. 2013 Aug 28;32(17 ):2336-47</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23921551</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2015 ;11(3):452-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25715028</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2005 Sep 23;122(6):927-39</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16179260</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Death Differ. 2015 Mar;22(3):367-76</Citation>
<ArticleIdList><ArticleId IdType="pubmed">25257169</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2014 Apr;85(4):855-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24304882</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2016;12 (1):1-222</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26799652</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2011 Jun;79(12):1361-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21430640</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Int Urol Nephrol. 2012 Aug;44(4):1251-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22213063</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2006 Apr;17(4):1135-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16495381</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2007 May;71(10):967-70</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17342180</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2010 Dec;78(12 ):1240-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20861825</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Circulation. 2002 Mar 5;105(9):1135-43</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11877368</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 2003 Jun;111(12):1805-12</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12813013</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Hypertension. 2010 Apr;55(4):953-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20157054</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Semin Nephrol. 2014 Jan;34(1):62-71</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24485031</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Cancer Res. 2012;2(2):214-21</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22485198</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2014 Feb;25(2):305-15</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24179166</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2011 Jan;22(1):124-36</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21115613</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Nephrol. 2011;34(3):203-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21791916</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>N Engl J Med. 2013 Feb 14;368(7):651-62</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23406030</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Med. 2000 Apr 1;108(5):403-15</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10759097</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2016 Aug;27(8):2331-45</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26701976</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2008 Feb 28;451(7182):1069-75</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18305538</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2014 Dec;25(12 ):2835-46</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24854279</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Annu Rev Cell Dev Biol. 2011;27:107-32</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21801009</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Autophagy. 2007 Sep-Oct;3(5):452-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17534139</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2013 Feb;24(2):268-82</Citation>
<ArticleIdList><ArticleId IdType="pubmed">23334396</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Clin J Am Soc Nephrol. 2011 May;6(5):966-73</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21393482</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2006 Apr;17(4):1143-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16495376</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Am J Physiol Renal Physiol. 2007 Aug;293(2):F476-85</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17475898</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Lab Invest. 2011 Jun;91(6):837-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21383672</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>BMC Nephrol. 2011 Jun 29;12:30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21714897</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2011 May;22(5):902-13</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21493778</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell Res. 2014 Jan;24(1):9-23</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24366340</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Intensive Care Med. 2015 Sep;41(9):1648-57</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26156107</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Am Soc Nephrol. 2014 Mar;25(3):595-605</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24503241</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Biol Cell. 2004 Mar;15(3):1101-11</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14699058</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Mol Cell Biol. 2005 Jun;6(6):505-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15928714</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Mol Cell Biol. 2007 Sep;8(9):741-52</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17717517</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Kidney Int. 2012 Dec;82(12 ):1271-83</Citation>
<ArticleIdList><ArticleId IdType="pubmed">22854643</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Clin J Am Soc Nephrol. 2015 Sep 4;10(9):1510-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">26231194</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Semin Nephrol. 2014 Jan;34(1):17-26</Citation>
<ArticleIdList><ArticleId IdType="pubmed">24485026</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Diabetologia. 2011 Oct;54(10):2713-23</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21744073</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
<region><li>Texas</li>
</region>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Bian, Ao" sort="Bian, Ao" uniqKey="Bian A" first="Ao" last="Bian">Ao Bian</name>
</noRegion>
<name sortKey="Li, Peng" sort="Li, Peng" uniqKey="Li P" first="Peng" last="Li">Peng Li</name>
<name sortKey="Xing, Changying" sort="Xing, Changying" uniqKey="Xing C" first="Changying" last="Xing">Changying Xing</name>
</country>
<country name="États-Unis"><region name="Texas"><name sortKey="Bian, Ao" sort="Bian, Ao" uniqKey="Bian A" first="Ao" last="Bian">Ao Bian</name>
</region>
<name sortKey="Flores, Brianna" sort="Flores, Brianna" uniqKey="Flores B" first="Brianna" last="Flores">Brianna Flores</name>
<name sortKey="Gillings, Nancy" sort="Gillings, Nancy" uniqKey="Gillings N" first="Nancy" last="Gillings">Nancy Gillings</name>
<name sortKey="Hu, Ming Chang" sort="Hu, Ming Chang" uniqKey="Hu M" first="Ming Chang" last="Hu">Ming Chang Hu</name>
<name sortKey="Hu, Ming Chang" sort="Hu, Ming Chang" uniqKey="Hu M" first="Ming Chang" last="Hu">Ming Chang Hu</name>
<name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
<name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
<name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
<name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
<name sortKey="Shi, Mingjun" sort="Shi, Mingjun" uniqKey="Shi M" first="Mingjun" last="Shi">Mingjun Shi</name>
<name sortKey="Yan, Shirley Xiao" sort="Yan, Shirley Xiao" uniqKey="Yan S" first="Shirley Xiao" last="Yan">Shirley Xiao Yan</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000870 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000870 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    RapamycinFungusV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:28886014
   |texte=   Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:28886014" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a RapamycinFungusV1

This area was generated with Dilib version V0.6.38.
Data generation: Thu Nov 19 21:55:41 2020. Site generation: Thu Nov 19 22:00:39 2020

	Serveur d'exploration sur la rapamycine et les champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la rapamycine et les champignons

Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.

Downregulation of autophagy is associated with severe ischemia-reperfusion-induced acute kidney injury in overexpressing C-reactive protein mice.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki