The protective effect of glutaredoxin 1/DJ-1/HSP70 signaling in renal tubular epithelial cells injury induced by ischemia.
Identifieur interne : 000110 ( Main/Exploration ); précédent : 000109; suivant : 000111The protective effect of glutaredoxin 1/DJ-1/HSP70 signaling in renal tubular epithelial cells injury induced by ischemia.
Auteurs : Jian Yin [République populaire de Chine] ; Ruisi Xu [République populaire de Chine] ; Jun Wei [République populaire de Chine] ; Siqi Zhang [République populaire de Chine]Source :
- Life sciences [ 1879-0631 ] ; 2019.
Descripteurs français
- KwdFr :
- Cellules épithéliales (métabolisme), Glucose (métabolisme), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Humains (MeSH), Ischémie (métabolisme), Lignée cellulaire (MeSH), Milieux de culture (MeSH), Oxygène (métabolisme), Protein deglycase DJ-1 (métabolisme), Protéines du choc thermique HSP70 (métabolisme), Régulation négative (MeSH), Stress oxydatif (MeSH), Techniques de culture cellulaire (MeSH), Transduction du signal (MeSH), Tubules rénaux (métabolisme), Tubules rénaux (vascularisation).
- MESH :
- génétique : Glutarédoxines.
- métabolisme : Cellules épithéliales, Glucose, Glutarédoxines, Ischémie, Oxygène, Protein deglycase DJ-1, Protéines du choc thermique HSP70, Tubules rénaux.
- vascularisation : Tubules rénaux.
- Humains, Lignée cellulaire, Milieux de culture, Régulation négative, Stress oxydatif, Techniques de culture cellulaire, Transduction du signal.
English descriptors
- KwdEn :
- Cell Culture Techniques (MeSH), Cell Line (MeSH), Culture Media (MeSH), Down-Regulation (MeSH), Epithelial Cells (metabolism), Glucose (metabolism), Glutaredoxins (genetics), Glutaredoxins (metabolism), HSP70 Heat-Shock Proteins (metabolism), Humans (MeSH), Ischemia (metabolism), Kidney Tubules (blood supply), Kidney Tubules (metabolism), Oxidative Stress (MeSH), Oxygen (metabolism), Protein Deglycase DJ-1 (metabolism), Signal Transduction (MeSH).
- MESH :
- chemical , genetics : Glutaredoxins.
- chemical , metabolism : Glucose, Glutaredoxins, HSP70 Heat-Shock Proteins, Oxygen, Protein Deglycase DJ-1.
- chemical : Culture Media.
- blood supply : Kidney Tubules.
- metabolism : Epithelial Cells, Ischemia, Kidney Tubules.
- Cell Culture Techniques, Cell Line, Down-Regulation, Humans, Oxidative Stress, Signal Transduction.
Abstract
AIMS
Gluaredoxin1 (GRX1) is an important protein of the cellular antioxidant defense system, but its role in renal epithelial cell injury caused by ischemia remains unclear. In this study, we aimed to gain insight into the role of GRX1 in HK-2 cells with oxygen glucose deprivation (OGD) injury, which served as an in vitro cell model of renal epithelial cell ischemic injury. We investigated the underlying regulation of GRX1, DJ-1, and HSP70 as well as the role of the GRX1/DJ-1/HSP70 signaling pathway in this model.
MATERIALS AND METHODS
The protein and mRNA expressions were measured by Western blot and qRT-PCR assays, respectively. GRX1 was overexpressed by transfection of pcDNA.3.1-GRX1 and DJ-1 was inhibited by transfection with DJ-1 siRNA. Cell apoptosis, caspase-3 activity, lactate dehydrogenase (LDH) leakage, or superoxide dismutase (SOD) content was tested by the related detection kit. Reactive oxygen species (ROS) level was detected via carboxy-H
KEY FINDINGS
We found that GRX1 was distinctly down-regulated in HK-2 cells after incubation under the OGD condition. GRX1 overexpression markedly constrained cell apoptosis, caspase-3 activity, LDH leakage, and the ROS level, while SOD content was elevated. GRX1 up-regulation increased DJ-1 and HSP70 protein expression, while DJ-1 inhibition significantly offset the effect of GRX1 overexpression on HSP70, indicating that GRX1 could regulate HSP70 via control of DJ-1. Moreover, we observed that HSP70 inhibition removed the constraints imposed by GRX1 overexpression on ROS level, LDH leakage, and caspase-3 activity.
SIGNIFICANCE
Overall, this study showed that GRX1 minimizes cell injury and apoptosis in HK-2 cells under OGD conditions via regulation of DJ-1 and HSP70 expression.
DOI: 10.1016/j.lfs.2019.03.015
PubMed: 30858124
Affiliations:
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Electronic address: zhgsiqi_sq843@163.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, China-Japan Union Hospital of Jilin University, Changchun 130033</wicri:regionArea><placeName><settlement type="city">Changchun</settlement><region type="province">Jilin</region><region type="groupement">Dongbei</region></placeName></affiliation></author></analytic><series><title level="j">Life sciences</title><idno type="eISSN">1879-0631</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Culture Techniques (MeSH)</term><term>Cell Line (MeSH)</term><term>Culture Media (MeSH)</term><term>Down-Regulation (MeSH)</term><term>Epithelial Cells (metabolism)</term><term>Glucose (metabolism)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>HSP70 Heat-Shock Proteins (metabolism)</term><term>Humans (MeSH)</term><term>Ischemia (metabolism)</term><term>Kidney Tubules (blood supply)</term><term>Kidney Tubules (metabolism)</term><term>Oxidative Stress (MeSH)</term><term>Oxygen (metabolism)</term><term>Protein Deglycase DJ-1 (metabolism)</term><term>Signal Transduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Cellules épithéliales (métabolisme)</term><term>Glucose (métabolisme)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Humains (MeSH)</term><term>Ischémie (métabolisme)</term><term>Lignée cellulaire (MeSH)</term><term>Milieux de culture (MeSH)</term><term>Oxygène (métabolisme)</term><term>Protein deglycase DJ-1 (métabolisme)</term><term>Protéines du choc thermique HSP70 (métabolisme)</term><term>Régulation négative (MeSH)</term><term>Stress oxydatif (MeSH)</term><term>Techniques de culture cellulaire (MeSH)</term><term>Transduction du signal (MeSH)</term><term>Tubules rénaux (métabolisme)</term><term>Tubules rénaux (vascularisation)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glucose</term><term>Glutaredoxins</term><term>HSP70 Heat-Shock Proteins</term><term>Oxygen</term><term>Protein Deglycase DJ-1</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Culture Media</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Kidney Tubules</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term><term>Ischemia</term><term>Kidney Tubules</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term><term>Glucose</term><term>Glutarédoxines</term><term>Ischémie</term><term>Oxygène</term><term>Protein deglycase DJ-1</term><term>Protéines du choc thermique HSP70</term><term>Tubules rénaux</term></keywords><keywords scheme="MESH" qualifier="vascularisation" xml:lang="fr"><term>Tubules rénaux</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Culture Techniques</term><term>Cell Line</term><term>Down-Regulation</term><term>Humans</term><term>Oxidative Stress</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term><term>Lignée cellulaire</term><term>Milieux de culture</term><term>Régulation négative</term><term>Stress oxydatif</term><term>Techniques de culture cellulaire</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>AIMS</b></p><p>Gluaredoxin1 (GRX1) is an important protein of the cellular antioxidant defense system, but its role in renal epithelial cell injury caused by ischemia remains unclear. In this study, we aimed to gain insight into the role of GRX1 in HK-2 cells with oxygen glucose deprivation (OGD) injury, which served as an in vitro cell model of renal epithelial cell ischemic injury. We investigated the underlying regulation of GRX1, DJ-1, and HSP70 as well as the role of the GRX1/DJ-1/HSP70 signaling pathway in this model.</p></div><div type="abstract" xml:lang="en"><p><b>MATERIALS AND METHODS</b></p><p>The protein and mRNA expressions were measured by Western blot and qRT-PCR assays, respectively. GRX1 was overexpressed by transfection of pcDNA.3.1-GRX1 and DJ-1 was inhibited by transfection with DJ-1 siRNA. Cell apoptosis, caspase-3 activity, lactate dehydrogenase (LDH) leakage, or superoxide dismutase (SOD) content was tested by the related detection kit. Reactive oxygen species (ROS) level was detected via carboxy-H</p></div><div type="abstract" xml:lang="en"><p><b>KEY FINDINGS</b></p><p>We found that GRX1 was distinctly down-regulated in HK-2 cells after incubation under the OGD condition. GRX1 overexpression markedly constrained cell apoptosis, caspase-3 activity, LDH leakage, and the ROS level, while SOD content was elevated. GRX1 up-regulation increased DJ-1 and HSP70 protein expression, while DJ-1 inhibition significantly offset the effect of GRX1 overexpression on HSP70, indicating that GRX1 could regulate HSP70 via control of DJ-1. Moreover, we observed that HSP70 inhibition removed the constraints imposed by GRX1 overexpression on ROS level, LDH leakage, and caspase-3 activity.</p></div><div type="abstract" xml:lang="en"><p><b>SIGNIFICANCE</b></p><p>Overall, this study showed that GRX1 minimizes cell injury and apoptosis in HK-2 cells under OGD conditions via regulation of DJ-1 and HSP70 expression.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30858124</PMID><DateCompleted><Year>2019</Year><Month>04</Month><Day>17</Day></DateCompleted><DateRevised><Year>2019</Year><Month>04</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0631</ISSN><JournalIssue CitedMedium="Internet"><Volume>223</Volume><PubDate><Year>2019</Year><Month>Apr</Month><Day>15</Day></PubDate></JournalIssue><Title>Life sciences</Title><ISOAbbreviation>Life Sci</ISOAbbreviation></Journal><ArticleTitle>The protective effect of glutaredoxin 1/DJ-1/HSP70 signaling in renal tubular epithelial cells injury induced by ischemia.</ArticleTitle><Pagination><MedlinePgn>88-94</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0024-3205(19)30173-0</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.lfs.2019.03.015</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">Gluaredoxin1 (GRX1) is an important protein of the cellular antioxidant defense system, but its role in renal epithelial cell injury caused by ischemia remains unclear. In this study, we aimed to gain insight into the role of GRX1 in HK-2 cells with oxygen glucose deprivation (OGD) injury, which served as an in vitro cell model of renal epithelial cell ischemic injury. We investigated the underlying regulation of GRX1, DJ-1, and HSP70 as well as the role of the GRX1/DJ-1/HSP70 signaling pathway in this model.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">The protein and mRNA expressions were measured by Western blot and qRT-PCR assays, respectively. GRX1 was overexpressed by transfection of pcDNA.3.1-GRX1 and DJ-1 was inhibited by transfection with DJ-1 siRNA. Cell apoptosis, caspase-3 activity, lactate dehydrogenase (LDH) leakage, or superoxide dismutase (SOD) content was tested by the related detection kit. Reactive oxygen species (ROS) level was detected via carboxy-H<sub>2</sub>DCF-DA.</AbstractText><AbstractText Label="KEY FINDINGS" NlmCategory="RESULTS">We found that GRX1 was distinctly down-regulated in HK-2 cells after incubation under the OGD condition. GRX1 overexpression markedly constrained cell apoptosis, caspase-3 activity, LDH leakage, and the ROS level, while SOD content was elevated. GRX1 up-regulation increased DJ-1 and HSP70 protein expression, while DJ-1 inhibition significantly offset the effect of GRX1 overexpression on HSP70, indicating that GRX1 could regulate HSP70 via control of DJ-1. Moreover, we observed that HSP70 inhibition removed the constraints imposed by GRX1 overexpression on ROS level, LDH leakage, and caspase-3 activity.</AbstractText><AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">Overall, this study showed that GRX1 minimizes cell injury and apoptosis in HK-2 cells under OGD conditions via regulation of DJ-1 and HSP70 expression.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yin</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Vascular Surgery, China-Japan Union Hospital of Jilin University, Changchun 130033, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Ruisi</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130033, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wei</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pharmacology Base, China-Japan Union Hospital of Jilin University, Changchun 130033, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Siqi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Nephrology, China-Japan Union Hospital of Jilin University, Changchun 130033, China. Electronic address: zhgsiqi_sq843@163.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>03</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Life Sci</MedlineTA><NlmUniqueID>0375521</NlmUniqueID><ISSNLinking>0024-3205</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003470">Culture Media</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018840">HSP70 Heat-Shock Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.2.-</RegistryNumber><NameOfSubstance UI="C105131">PARK7 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.2.-</RegistryNumber><NameOfSubstance UI="D000071617">Protein Deglycase DJ-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D018929" MajorTopicYN="N">Cell Culture Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003470" MajorTopicYN="N">Culture Media</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018840" MajorTopicYN="N">HSP70 Heat-Shock Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007511" MajorTopicYN="N">Ischemia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007684" MajorTopicYN="N">Kidney Tubules</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="Y">blood supply</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010100" MajorTopicYN="N">Oxygen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071617" MajorTopicYN="N">Protein Deglycase DJ-1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DJ-1</Keyword><Keyword MajorTopicYN="N">GRX1</Keyword><Keyword MajorTopicYN="N">HK-2</Keyword><Keyword MajorTopicYN="N">HSP70</Keyword><Keyword MajorTopicYN="N">OGD</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>02</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>03</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>3</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>4</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>3</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">30858124</ArticleId><ArticleId IdType="pii">S0024-3205(19)30173-0</ArticleId><ArticleId IdType="doi">10.1016/j.lfs.2019.03.015</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><region><li>Dongbei</li><li>Jilin</li></region><settlement><li>Changchun</li></settlement></list><tree><country name="République populaire de Chine"><region name="Jilin"><name sortKey="Yin, Jian" sort="Yin, Jian" uniqKey="Yin J" first="Jian" last="Yin">Jian Yin</name></region><name sortKey="Wei, Jun" sort="Wei, Jun" uniqKey="Wei J" first="Jun" last="Wei">Jun Wei</name><name sortKey="Xu, Ruisi" sort="Xu, Ruisi" uniqKey="Xu R" first="Ruisi" last="Xu">Ruisi Xu</name><name sortKey="Zhang, Siqi" sort="Zhang, Siqi" uniqKey="Zhang S" first="Siqi" last="Zhang">Siqi Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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