Sulfiredoxin-1 alleviates high glucose-induced podocyte injury though promoting Nrf2/ARE signaling via inactivation of GSK-3β.
Identifieur interne : 000083 ( Main/Exploration ); précédent : 000082; suivant : 000084Sulfiredoxin-1 alleviates high glucose-induced podocyte injury though promoting Nrf2/ARE signaling via inactivation of GSK-3β.
Auteurs : Yan Shen [République populaire de Chine] ; Shengnan Chen [République populaire de Chine] ; Yan Zhao [République populaire de Chine]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2019.
Descripteurs français
- KwdFr :
- Activation enzymatique (MeSH), Animaux (MeSH), Facteur-2 apparenté à NF-E2 (métabolisme), Glucose (métabolisme), Glycogen synthase kinase 3 beta (métabolisme), Lignée cellulaire (MeSH), Néphropathies diabétiques (métabolisme), Oxidoreductases acting on sulfur group donors (métabolisme), Podocytes (métabolisme), Souris (MeSH), Transduction du signal (MeSH), Éléments de réponse aux anti-oxydants (MeSH).
- MESH :
English descriptors
- KwdEn :
- Animals (MeSH), Antioxidant Response Elements (MeSH), Cell Line (MeSH), Diabetic Nephropathies (metabolism), Enzyme Activation (MeSH), Glucose (metabolism), Glycogen Synthase Kinase 3 beta (metabolism), Mice (MeSH), NF-E2-Related Factor 2 (metabolism), Oxidoreductases Acting on Sulfur Group Donors (metabolism), Podocytes (metabolism), Signal Transduction (MeSH).
- MESH :
- chemical , metabolism : Glucose, Glycogen Synthase Kinase 3 beta, NF-E2-Related Factor 2, Oxidoreductases Acting on Sulfur Group Donors.
- metabolism : Diabetic Nephropathies, Podocytes.
- Animals, Antioxidant Response Elements, Cell Line, Enzyme Activation, Mice, Signal Transduction.
Abstract
Hyperglycemia-induced podocyte injury plays a vital role in the development of diabetic nephropathy. Sulfiredoxin-1 (Srxn1) is emerging as a cytoprotective protein that protects from various insults in a wide range of cell types. However, whether Srxn1 is involved in regulating hyperglycemia-induced podocyte injury and participates in diabetic nephropathy remains unknown. In the present study, we aimed to explore the potential role of Srxn1 in regulating high glucose (HG)-induced apoptosis and oxidative stress of podocytes in vitro. Results demonstrated that Srxn1 was induced in HG-stimulated podocytes. The depletion of Srxn1 by Srxn1 siRNA-mediated gene silencing significantly exacerbated HG-induced apoptosis and the production of reactive oxygen species (ROS), while Srxn1 overexpression attenuated HG-induced apoptosis and ROS production. In-depth molecular mechanism research revealed that Srxn1 overexpression promoted the nuclear expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and reinforced antioxidant response element (ARE)-mediated transcription activity. Moreover, results confirmed that Srxn1 increased the activation of Nrf2/ARE signaling associated with inactivating glycogen synthase kinase (GSK)-3β. Notably, the inhibition of GSK-3β significantly reversed Srxn1 silencing-induced adverse effects in HG-treated cells, while the knockdown of Nrf2 abrogated the Srxn1-mediated protective effect against HG-induced podocyte injury. Taken together, our results demonstrated that Srxn1 protects podocytes from HG-induced injury by promoting the activation of Nrf2/ARE signaling associated with inactivating GSK-3β, indicating a potential role of Srxn1 in diabetic nephropathy. Our study suggests that Srxn1 may serve as a potential target for kidney protection.
DOI: 10.1016/j.bbrc.2019.06.157
PubMed: 31284950
Affiliations:
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Le document en format XML
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Electronic address: shenyan696@126.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061</wicri:regionArea><wicri:noRegion>710061</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Shengnan" sort="Chen, Shengnan" uniqKey="Chen S" first="Shengnan" last="Chen">Shengnan Chen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061</wicri:regionArea><wicri:noRegion>710061</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061</wicri:regionArea><wicri:noRegion>710061</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31284950</idno><idno type="pmid">31284950</idno><idno type="doi">10.1016/j.bbrc.2019.06.157</idno><idno type="wicri:Area/Main/Corpus">000109</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000109</idno><idno type="wicri:Area/Main/Curation">000109</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000109</idno><idno type="wicri:Area/Main/Exploration">000109</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Sulfiredoxin-1 alleviates high glucose-induced podocyte injury though promoting Nrf2/ARE signaling via inactivation of GSK-3β.</title><author><name sortKey="Shen, Yan" sort="Shen, Yan" uniqKey="Shen Y" first="Yan" last="Shen">Yan Shen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China. Electronic address: shenyan696@126.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061</wicri:regionArea><wicri:noRegion>710061</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Shengnan" sort="Chen, Shengnan" uniqKey="Chen S" first="Shengnan" last="Chen">Shengnan Chen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061</wicri:regionArea><wicri:noRegion>710061</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061</wicri:regionArea><wicri:noRegion>710061</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Antioxidant Response Elements (MeSH)</term><term>Cell Line (MeSH)</term><term>Diabetic Nephropathies (metabolism)</term><term>Enzyme Activation (MeSH)</term><term>Glucose (metabolism)</term><term>Glycogen Synthase Kinase 3 beta (metabolism)</term><term>Mice (MeSH)</term><term>NF-E2-Related Factor 2 (metabolism)</term><term>Oxidoreductases Acting on Sulfur Group Donors (metabolism)</term><term>Podocytes (metabolism)</term><term>Signal Transduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation enzymatique (MeSH)</term><term>Animaux (MeSH)</term><term>Facteur-2 apparenté à NF-E2 (métabolisme)</term><term>Glucose (métabolisme)</term><term>Glycogen synthase kinase 3 beta (métabolisme)</term><term>Lignée cellulaire (MeSH)</term><term>Néphropathies diabétiques (métabolisme)</term><term>Oxidoreductases acting on sulfur group donors (métabolisme)</term><term>Podocytes (métabolisme)</term><term>Souris (MeSH)</term><term>Transduction du signal (MeSH)</term><term>Éléments de réponse aux anti-oxydants (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glucose</term><term>Glycogen Synthase Kinase 3 beta</term><term>NF-E2-Related Factor 2</term><term>Oxidoreductases Acting on Sulfur Group Donors</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Diabetic Nephropathies</term><term>Podocytes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term><term>Glucose</term><term>Glycogen synthase kinase 3 beta</term><term>Néphropathies diabétiques</term><term>Oxidoreductases acting on sulfur group donors</term><term>Podocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Antioxidant Response Elements</term><term>Cell Line</term><term>Enzyme Activation</term><term>Mice</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term><term>Animaux</term><term>Lignée cellulaire</term><term>Souris</term><term>Transduction du signal</term><term>Éléments de réponse aux anti-oxydants</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Hyperglycemia-induced podocyte injury plays a vital role in the development of diabetic nephropathy. Sulfiredoxin-1 (Srxn1) is emerging as a cytoprotective protein that protects from various insults in a wide range of cell types. However, whether Srxn1 is involved in regulating hyperglycemia-induced podocyte injury and participates in diabetic nephropathy remains unknown. In the present study, we aimed to explore the potential role of Srxn1 in regulating high glucose (HG)-induced apoptosis and oxidative stress of podocytes in vitro. Results demonstrated that Srxn1 was induced in HG-stimulated podocytes. The depletion of Srxn1 by Srxn1 siRNA-mediated gene silencing significantly exacerbated HG-induced apoptosis and the production of reactive oxygen species (ROS), while Srxn1 overexpression attenuated HG-induced apoptosis and ROS production. In-depth molecular mechanism research revealed that Srxn1 overexpression promoted the nuclear expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and reinforced antioxidant response element (ARE)-mediated transcription activity. Moreover, results confirmed that Srxn1 increased the activation of Nrf2/ARE signaling associated with inactivating glycogen synthase kinase (GSK)-3β. Notably, the inhibition of GSK-3β significantly reversed Srxn1 silencing-induced adverse effects in HG-treated cells, while the knockdown of Nrf2 abrogated the Srxn1-mediated protective effect against HG-induced podocyte injury. Taken together, our results demonstrated that Srxn1 protects podocytes from HG-induced injury by promoting the activation of Nrf2/ARE signaling associated with inactivating GSK-3β, indicating a potential role of Srxn1 in diabetic nephropathy. Our study suggests that Srxn1 may serve as a potential target for kidney protection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31284950</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>01</Day></DateCompleted><DateRevised><Year>2020</Year><Month>06</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><Volume>516</Volume><Issue>4</Issue><PubDate><Year>2019</Year><Month>09</Month><Day>03</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Sulfiredoxin-1 alleviates high glucose-induced podocyte injury though promoting Nrf2/ARE signaling via inactivation of GSK-3β.</ArticleTitle><Pagination><MedlinePgn>1137-1144</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(19)31317-8</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2019.06.157</ELocationID><Abstract><AbstractText>Hyperglycemia-induced podocyte injury plays a vital role in the development of diabetic nephropathy. Sulfiredoxin-1 (Srxn1) is emerging as a cytoprotective protein that protects from various insults in a wide range of cell types. However, whether Srxn1 is involved in regulating hyperglycemia-induced podocyte injury and participates in diabetic nephropathy remains unknown. In the present study, we aimed to explore the potential role of Srxn1 in regulating high glucose (HG)-induced apoptosis and oxidative stress of podocytes in vitro. Results demonstrated that Srxn1 was induced in HG-stimulated podocytes. The depletion of Srxn1 by Srxn1 siRNA-mediated gene silencing significantly exacerbated HG-induced apoptosis and the production of reactive oxygen species (ROS), while Srxn1 overexpression attenuated HG-induced apoptosis and ROS production. In-depth molecular mechanism research revealed that Srxn1 overexpression promoted the nuclear expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and reinforced antioxidant response element (ARE)-mediated transcription activity. Moreover, results confirmed that Srxn1 increased the activation of Nrf2/ARE signaling associated with inactivating glycogen synthase kinase (GSK)-3β. Notably, the inhibition of GSK-3β significantly reversed Srxn1 silencing-induced adverse effects in HG-treated cells, while the knockdown of Nrf2 abrogated the Srxn1-mediated protective effect against HG-induced podocyte injury. Taken together, our results demonstrated that Srxn1 protects podocytes from HG-induced injury by promoting the activation of Nrf2/ARE signaling associated with inactivating GSK-3β, indicating a potential role of Srxn1 in diabetic nephropathy. Our study suggests that Srxn1 may serve as a potential target for kidney protection.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shen</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China. Electronic address: shenyan696@126.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Shengnan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Nephrology, Kidney Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Yan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.</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 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