AustralieFrV1, PubMed, Checkpoint, bibRecord, 003846

Ablation of proximal tubular suppressor of cytokine signaling 3 enhances tubular cell cycling and modifies macrophage phenotype during acute kidney injury.

Identifieur interne : 003846 ( PubMed/Checkpoint ); précédent : 003845; suivant : 003847

Ablation of proximal tubular suppressor of cytokine signaling 3 enhances tubular cell cycling and modifies macrophage phenotype during acute kidney injury.

Auteurs : Nathan Susnik [Allemagne] ; Inga Sörensen-Zender [Allemagne] ; Song Rong [Allemagne] ; Sibylle Von Vietinghoff [Allemagne] ; Xia Lu [Allemagne] ; Isabelle Rubera [France] ; Michel Tauc [France] ; Christine S. Falk [Allemagne] ; Warren S. Alexander [Australie] ; Anette Melk [Allemagne] ; Herrmann Haller [Allemagne] ; Roland Schmitt [Allemagne]

Source :

Kidney international [ 1523-1755 ] ; 2014.

RBID : pubmed:24402091

Descripteurs français

English descriptors

KwdEn :
- Acute Kidney Injury (genetics), Acute Kidney Injury (immunology), Acute Kidney Injury (metabolism), Acute Kidney Injury (pathology), Acute Kidney Injury (physiopathology), Animals, Antigens, Differentiation (metabolism), Cell Proliferation, Cells, Cultured, Coculture Techniques, Disease Models, Animal, Gene Expression Regulation, Genotype, Janus Kinases (metabolism), Kidney Tubules, Proximal (immunology), Kidney Tubules, Proximal (metabolism), Kidney Tubules, Proximal (pathology), Kidney Tubules, Proximal (physiopathology), Macrophage Activation, Macrophages (immunology), Macrophages (metabolism), Male, Mice, Inbred C57BL, Mice, Knockout, Phenotype, RNA Interference, STAT Transcription Factors (metabolism), Signal Transduction, Suppressor of Cytokine Signaling 3 Protein, Suppressor of Cytokine Signaling Proteins (deficiency), Suppressor of Cytokine Signaling Proteins (genetics), Time Factors, Transfection.
MESH :
- chemical , deficiency : Suppressor of Cytokine Signaling Proteins.
- chemical , genetics : Suppressor of Cytokine Signaling Proteins.
- chemical , metabolism : Antigens, Differentiation, Janus Kinases, STAT Transcription Factors.
- genetics : Acute Kidney Injury.
- immunology : Acute Kidney Injury, Kidney Tubules, Proximal, Macrophages.
- metabolism : Acute Kidney Injury, Kidney Tubules, Proximal, Macrophages.
- pathology : Acute Kidney Injury, Kidney Tubules, Proximal.
- physiopathology : Acute Kidney Injury, Kidney Tubules, Proximal.
- Animals, Cell Proliferation, Cells, Cultured, Coculture Techniques, Disease Models, Animal, Gene Expression Regulation, Genotype, Macrophage Activation, Male, Mice, Inbred C57BL, Mice, Knockout, Phenotype, RNA Interference, Signal Transduction, Suppressor of Cytokine Signaling 3 Protein, Time Factors, Transfection.

Abstract

Suppressor of cytokine signaling 3 (SOCS-3) is an important intracellular negative regulator of several signaling pathways. We found that SOCS-3 is highly expressed in renal proximal tubules during acute kidney injury. To test the impact of this, conditional proximal tubular knockout mice (SOCS-3(sglt2Δ/sglt2Δ)) were created. These mice had better kidney function than their wild-type counterparts in aristolochic acid nephropathy and after ischemia/reperfusion injury. Kidneys of these knockout mice showed significantly more proximal tubular cell proliferation during the repair phase. A direct effect of SOCS-3 on tubular cell cycling was demonstrated by in vitro experiments showing a JAK/STAT pathway-dependent antimitotic effect of SOCS-3. Furthermore, acute damaged kidneys of the knockout mice contained increased numbers of F4/80(+) cells. Phenotypic analysis of these F4/80(+) cells indicated a polarization from classically activated to alternatively activated macrophages. In vitro, SOCS-3-overexpressing renal epithelial cells directly induced classical activation in cocultured macrophages, supporting the observed in vivo phenomenon. Thus, upregulation of SOCS-3 in stressed proximal tubules plays an important role during acute kidney injury by inhibition of reparative proliferation and by modulation of the macrophage phenotype. Antagonizing SOCS-3 could have therapeutic potential for acute kidney injury.

DOI: 10.1038/ki.2013.525
PubMed: 24402091

Affiliations:

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<author><name sortKey="Alexander, Warren S" sort="Alexander, Warren S" uniqKey="Alexander W" first="Warren S" last="Alexander">Warren S. Alexander</name>
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<term>Acute Kidney Injury (immunology)</term>
<term>Acute Kidney Injury (metabolism)</term>
<term>Acute Kidney Injury (pathology)</term>
<term>Acute Kidney Injury (physiopathology)</term>
<term>Animals</term>
<term>Antigens, Differentiation (metabolism)</term>
<term>Cell Proliferation</term>
<term>Cells, Cultured</term>
<term>Coculture Techniques</term>
<term>Disease Models, Animal</term>
<term>Gene Expression Regulation</term>
<term>Genotype</term>
<term>Janus Kinases (metabolism)</term>
<term>Kidney Tubules, Proximal (immunology)</term>
<term>Kidney Tubules, Proximal (metabolism)</term>
<term>Kidney Tubules, Proximal (pathology)</term>
<term>Kidney Tubules, Proximal (physiopathology)</term>
<term>Macrophage Activation</term>
<term>Macrophages (immunology)</term>
<term>Macrophages (metabolism)</term>
<term>Male</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Phenotype</term>
<term>RNA Interference</term>
<term>STAT Transcription Factors (metabolism)</term>
<term>Signal Transduction</term>
<term>Suppressor of Cytokine Signaling 3 Protein</term>
<term>Suppressor of Cytokine Signaling Proteins (deficiency)</term>
<term>Suppressor of Cytokine Signaling Proteins (genetics)</term>
<term>Time Factors</term>
<term>Transfection</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation des macrophages</term>
<term>Animaux</term>
<term>Antigènes de différenciation (métabolisme)</term>
<term>Atteinte rénale aigüe (anatomopathologie)</term>
<term>Atteinte rénale aigüe (génétique)</term>
<term>Atteinte rénale aigüe (immunologie)</term>
<term>Atteinte rénale aigüe (métabolisme)</term>
<term>Atteinte rénale aigüe (physiopathologie)</term>
<term>Cellules cultivées</term>
<term>Facteurs de transcription STAT (métabolisme)</term>
<term>Facteurs temps</term>
<term>Génotype</term>
<term>Interférence par ARN</term>
<term>Janus kinases (métabolisme)</term>
<term>Macrophages (immunologie)</term>
<term>Macrophages (métabolisme)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Phénotype</term>
<term>Prolifération cellulaire</term>
<term>Protéine-3 suppressive de la signalisation des cytokine</term>
<term>Protéines SOCS (déficit)</term>
<term>Protéines SOCS (génétique)</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Techniques de coculture</term>
<term>Transduction du signal</term>
<term>Transfection</term>
<term>Tubules contournés proximaux (anatomopathologie)</term>
<term>Tubules contournés proximaux (immunologie)</term>
<term>Tubules contournés proximaux (métabolisme)</term>
<term>Tubules contournés proximaux (physiopathologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Suppressor of Cytokine Signaling Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Suppressor of Cytokine Signaling Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, Differentiation</term>
<term>Janus Kinases</term>
<term>STAT Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Atteinte rénale aigüe</term>
<term>Tubules contournés proximaux</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Protéines SOCS</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Acute Kidney Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Atteinte rénale aigüe</term>
<term>Protéines SOCS</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Atteinte rénale aigüe</term>
<term>Macrophages</term>
<term>Tubules contournés proximaux</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Acute Kidney Injury</term>
<term>Kidney Tubules, Proximal</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acute Kidney Injury</term>
<term>Kidney Tubules, Proximal</term>
<term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes de différenciation</term>
<term>Atteinte rénale aigüe</term>
<term>Facteurs de transcription STAT</term>
<term>Janus kinases</term>
<term>Macrophages</term>
<term>Tubules contournés proximaux</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Acute Kidney Injury</term>
<term>Kidney Tubules, Proximal</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Atteinte rénale aigüe</term>
<term>Tubules contournés proximaux</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Acute Kidney Injury</term>
<term>Kidney Tubules, Proximal</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Proliferation</term>
<term>Cells, Cultured</term>
<term>Coculture Techniques</term>
<term>Disease Models, Animal</term>
<term>Gene Expression Regulation</term>
<term>Genotype</term>
<term>Macrophage Activation</term>
<term>Male</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Phenotype</term>
<term>RNA Interference</term>
<term>Signal Transduction</term>
<term>Suppressor of Cytokine Signaling 3 Protein</term>
<term>Time Factors</term>
<term>Transfection</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des macrophages</term>
<term>Animaux</term>
<term>Cellules cultivées</term>
<term>Facteurs temps</term>
<term>Génotype</term>
<term>Interférence par ARN</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Phénotype</term>
<term>Prolifération cellulaire</term>
<term>Protéine-3 suppressive de la signalisation des cytokine</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris de lignée C57BL</term>
<term>Souris knockout</term>
<term>Techniques de coculture</term>
<term>Transduction du signal</term>
<term>Transfection</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Suppressor of cytokine signaling 3 (SOCS-3) is an important intracellular negative regulator of several signaling pathways. We found that SOCS-3 is highly expressed in renal proximal tubules during acute kidney injury. To test the impact of this, conditional proximal tubular knockout mice (SOCS-3(sglt2Δ/sglt2Δ)) were created. These mice had better kidney function than their wild-type counterparts in aristolochic acid nephropathy and after ischemia/reperfusion injury. Kidneys of these knockout mice showed significantly more proximal tubular cell proliferation during the repair phase. A direct effect of SOCS-3 on tubular cell cycling was demonstrated by in vitro experiments showing a JAK/STAT pathway-dependent antimitotic effect of SOCS-3. Furthermore, acute damaged kidneys of the knockout mice contained increased numbers of F4/80(+) cells. Phenotypic analysis of these F4/80(+) cells indicated a polarization from classically activated to alternatively activated macrophages. In vitro, SOCS-3-overexpressing renal epithelial cells directly induced classical activation in cocultured macrophages, supporting the observed in vivo phenomenon. Thus, upregulation of SOCS-3 in stressed proximal tubules plays an important role during acute kidney injury by inhibition of reparative proliferation and by modulation of the macrophage phenotype. Antagonizing SOCS-3 could have therapeutic potential for acute kidney injury.</div>
</front>
</TEI>
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<DateCreated><Year>2014</Year>
<Month>05</Month>
<Day>30</Day>
</DateCreated>
<DateCompleted><Year>2015</Year>
<Month>02</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>11</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1523-1755</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>85</Volume>
<Issue>6</Issue>
<PubDate><Year>2014</Year>
<Month>Jun</Month>
</PubDate>
</JournalIssue>
<Title>Kidney international</Title>
<ISOAbbreviation>Kidney Int.</ISOAbbreviation>
</Journal>
<ArticleTitle>Ablation of proximal tubular suppressor of cytokine signaling 3 enhances tubular cell cycling and modifies macrophage phenotype during acute kidney injury.</ArticleTitle>
<Pagination><MedlinePgn>1357-68</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/ki.2013.525</ELocationID>
<Abstract><AbstractText>Suppressor of cytokine signaling 3 (SOCS-3) is an important intracellular negative regulator of several signaling pathways. We found that SOCS-3 is highly expressed in renal proximal tubules during acute kidney injury. To test the impact of this, conditional proximal tubular knockout mice (SOCS-3(sglt2Δ/sglt2Δ)) were created. These mice had better kidney function than their wild-type counterparts in aristolochic acid nephropathy and after ischemia/reperfusion injury. Kidneys of these knockout mice showed significantly more proximal tubular cell proliferation during the repair phase. A direct effect of SOCS-3 on tubular cell cycling was demonstrated by in vitro experiments showing a JAK/STAT pathway-dependent antimitotic effect of SOCS-3. Furthermore, acute damaged kidneys of the knockout mice contained increased numbers of F4/80(+) cells. Phenotypic analysis of these F4/80(+) cells indicated a polarization from classically activated to alternatively activated macrophages. In vitro, SOCS-3-overexpressing renal epithelial cells directly induced classical activation in cocultured macrophages, supporting the observed in vivo phenomenon. Thus, upregulation of SOCS-3 in stressed proximal tubules plays an important role during acute kidney injury by inhibition of reparative proliferation and by modulation of the macrophage phenotype. Antagonizing SOCS-3 could have therapeutic potential for acute kidney injury.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Susnik</LastName>
<ForeName>Nathan</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sörensen-Zender</LastName>
<ForeName>Inga</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rong</LastName>
<ForeName>Song</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>von Vietinghoff</LastName>
<ForeName>Sibylle</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lu</LastName>
<ForeName>Xia</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rubera</LastName>
<ForeName>Isabelle</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>LP2M, CNRS 3472, University of Nice-Sophia Antipolis, Nice, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tauc</LastName>
<ForeName>Michel</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>LP2M, CNRS 3472, University of Nice-Sophia Antipolis, Nice, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Falk</LastName>
<ForeName>Christine S</ForeName>
<Initials>CS</Initials>
<AffiliationInfo><Affiliation>Institute of Transplant Immunology, Integrated Research and Treatment Center Transplantation, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Alexander</LastName>
<ForeName>Warren S</ForeName>
<Initials>WS</Initials>
<AffiliationInfo><Affiliation>The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Melk</LastName>
<ForeName>Anette</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Division of Pediatric Nephrology, Gastroenterology and Metabolic Diseases, Children's Hospital, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Haller</LastName>
<ForeName>Herrmann</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schmitt</LastName>
<ForeName>Roland</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Nephrology, Hannover Medical School, Hannover, Germany.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>01</Month>
<Day>08</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Kidney Int</MedlineTA>
<NlmUniqueID>0323470</NlmUniqueID>
<ISSNLinking>0085-2538</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000943">Antigens, Differentiation</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D050791">STAT Transcription Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C491411">Socs3 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000071223">Suppressor of Cytokine Signaling 3 Protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D050826">Suppressor of Cytokine Signaling Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C036763">monocyte-macrophage differentiation antigen</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.2</RegistryNumber>
<NameOfSubstance UI="D053612">Janus Kinases</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D058186" MajorTopicYN="N">Acute Kidney Injury</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000943" MajorTopicYN="N">Antigens, Differentiation</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018920" MajorTopicYN="N">Coculture Techniques</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName>
</MeshHeading>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D007687" MajorTopicYN="N">Kidney Tubules, Proximal</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008262" MajorTopicYN="N">Macrophage Activation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034622" MajorTopicYN="N">RNA Interference</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050791" MajorTopicYN="N">STAT Transcription Factors</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000071223" MajorTopicYN="N">Suppressor of Cytokine Signaling 3 Protein</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050826" MajorTopicYN="N">Suppressor of Cytokine Signaling Proteins</DescriptorName>
<QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName>
</MeshHeading>
</MeshHeadingList>
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<Month>11</Month>
<Day>13</Day>
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<PubMedPubDate PubStatus="revised"><Year>2013</Year>
<Month>09</Month>
<Day>18</Day>
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<PubMedPubDate PubStatus="accepted"><Year>2013</Year>
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<affiliations><list><country><li>Allemagne</li>
<li>Australie</li>
<li>France</li>
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<region><li>Basse-Saxe</li>
<li>Provence-Alpes-Côte d'Azur</li>
<li>Victoria (État)</li>
</region>
<settlement><li>Hanovre</li>
<li>Melbourne</li>
<li>Nice</li>
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<tree><country name="Allemagne"><region name="Basse-Saxe"><name sortKey="Susnik, Nathan" sort="Susnik, Nathan" uniqKey="Susnik N" first="Nathan" last="Susnik">Nathan Susnik</name>
</region>
<name sortKey="Falk, Christine S" sort="Falk, Christine S" uniqKey="Falk C" first="Christine S" last="Falk">Christine S. Falk</name>
<name sortKey="Haller, Herrmann" sort="Haller, Herrmann" uniqKey="Haller H" first="Herrmann" last="Haller">Herrmann Haller</name>
<name sortKey="Lu, Xia" sort="Lu, Xia" uniqKey="Lu X" first="Xia" last="Lu">Xia Lu</name>
<name sortKey="Melk, Anette" sort="Melk, Anette" uniqKey="Melk A" first="Anette" last="Melk">Anette Melk</name>
<name sortKey="Rong, Song" sort="Rong, Song" uniqKey="Rong S" first="Song" last="Rong">Song Rong</name>
<name sortKey="Schmitt, Roland" sort="Schmitt, Roland" uniqKey="Schmitt R" first="Roland" last="Schmitt">Roland Schmitt</name>
<name sortKey="Sorensen Zender, Inga" sort="Sorensen Zender, Inga" uniqKey="Sorensen Zender I" first="Inga" last="Sörensen-Zender">Inga Sörensen-Zender</name>
<name sortKey="Von Vietinghoff, Sibylle" sort="Von Vietinghoff, Sibylle" uniqKey="Von Vietinghoff S" first="Sibylle" last="Von Vietinghoff">Sibylle Von Vietinghoff</name>
</country>
<country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Rubera, Isabelle" sort="Rubera, Isabelle" uniqKey="Rubera I" first="Isabelle" last="Rubera">Isabelle Rubera</name>
</region>
<name sortKey="Tauc, Michel" sort="Tauc, Michel" uniqKey="Tauc M" first="Michel" last="Tauc">Michel Tauc</name>
</country>
<country name="Australie"><region name="Victoria (État)"><name sortKey="Alexander, Warren S" sort="Alexander, Warren S" uniqKey="Alexander W" first="Warren S" last="Alexander">Warren S. Alexander</name>
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</country>
</tree>
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Ablation of proximal tubular suppressor of cytokine signaling 3 enhances tubular cell cycling and modifies macrophage phenotype during acute kidney injury.

Ablation of proximal tubular suppressor of cytokine signaling 3 enhances tubular cell cycling and modifies macrophage phenotype during acute kidney injury.

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