Autophagy Dynamics and Modulation in a Rat Model of Renal Ischemia-Reperfusion Injury.
Identifieur interne : 000148 ( Main/Exploration ); précédent : 000147; suivant : 000149Autophagy Dynamics and Modulation in a Rat Model of Renal Ischemia-Reperfusion Injury.
Auteurs : Jean-Paul Decuypere [Belgique] ; Shawn Hutchinson [Belgique] ; Diethard Monbaliu [Belgique] ; Wim Martinet [Belgique] ; Jacques Pirenne [Belgique] ; Ina Jochmans [Belgique]Source :
- International journal of molecular sciences [ 1422-0067 ] ; 2020.
Abstract
Renal ischemia-reperfusion (IR) injury leading to cell death is a major cause of acute kidney injury, contributing to morbidity and mortality. Autophagy counteracts cell death by removing damaged macromolecules and organelles, making it an interesting anchor point for treatment strategies. However, autophagy is also suggested to enhance cell death when the ischemic burden is too strong. To investigate whether the role of autophagy depends on the severity of ischemic stress, we analyzed the dynamics of autophagy and apoptosis in an IR rat model with mild (45 min) or severe (60 min) renal ischemia. Following mild IR, renal injury was associated with reduced autophagy, enhanced mammalian target of rapamycin (mTOR) activity, and apoptosis. Severe IR, on the other hand, was associated with a higher autophagic activity, independent of mTOR, and without affecting apoptosis. Autophagy stimulation by trehalose injected 24 and 48 h prior to onset of severe ischemia did not reduce renal injury markers nor function, but reduced apoptosis and restored tubular dilation 7 days post reperfusion. This suggests that trehalose-dependent autophagy stimulation enhances tissue repair following an IR injury. Our data show that autophagy dynamics are strongly dependent on the severity of IR and that trehalose shows the potential to trigger autophagy-dependent repair processes following renal IR injury.
DOI: 10.3390/ijms21197185
PubMed: 33003356
PubMed Central: PMC7583807
Affiliations:
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first="Diethard" last="Monbaliu">Diethard Monbaliu</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven</wicri:regionArea><wicri:noRegion>B-3000 Leuven</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven</wicri:regionArea><wicri:noRegion>B-3000 Leuven</wicri:noRegion></affiliation></author><author><name sortKey="Martinet, Wim" sort="Martinet, Wim" uniqKey="Martinet W" first="Wim" last="Martinet">Wim Martinet</name><affiliation wicri:level="4"><nlm:affiliation>Department of Pharmaceutical Sciences, University of Antwerp, B-2610 Antwerp, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Department of Pharmaceutical Sciences, University of Antwerp, B-2610 Antwerp</wicri:regionArea><orgName type="university">Université d'Anvers</orgName><placeName><settlement type="city">Anvers</settlement><region>Région flamande</region><region type="district" nuts="2">Province d'Anvers</region></placeName></affiliation></author><author><name sortKey="Pirenne, Jacques" sort="Pirenne, Jacques" uniqKey="Pirenne J" first="Jacques" last="Pirenne">Jacques Pirenne</name><affiliation wicri:level="1"><nlm:affiliation>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven, Belgium.</nlm:affiliation><country 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Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven</wicri:regionArea><wicri:noRegion>B-3000 Leuven</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven</wicri:regionArea><wicri:noRegion>B-3000 Leuven</wicri:noRegion></affiliation></author></analytic><series><title level="j">International journal of molecular sciences</title><idno type="eISSN">1422-0067</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Renal ischemia-reperfusion (IR) injury leading to cell death is a major cause of acute kidney injury, contributing to morbidity and mortality. Autophagy counteracts cell death by removing damaged macromolecules and organelles, making it an interesting anchor point for treatment strategies. However, autophagy is also suggested to enhance cell death when the ischemic burden is too strong. To investigate whether the role of autophagy depends on the severity of ischemic stress, we analyzed the dynamics of autophagy and apoptosis in an IR rat model with mild (45 min) or severe (60 min) renal ischemia. Following mild IR, renal injury was associated with reduced autophagy, enhanced mammalian target of rapamycin (mTOR) activity, and apoptosis. Severe IR, on the other hand, was associated with a higher autophagic activity, independent of mTOR, and without affecting apoptosis. Autophagy stimulation by trehalose injected 24 and 48 h prior to onset of severe ischemia did not reduce renal injury markers nor function, but reduced apoptosis and restored tubular dilation 7 days post reperfusion. This suggests that trehalose-dependent autophagy stimulation enhances tissue repair following an IR injury. Our data show that autophagy dynamics are strongly dependent on the severity of IR and that trehalose shows the potential to trigger autophagy-dependent repair processes following renal IR injury.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">33003356</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>29</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1422-0067</ISSN><JournalIssue CitedMedium="Internet"><Volume>21</Volume><Issue>19</Issue><PubDate><Year>2020</Year><Month>Sep</Month><Day>29</Day></PubDate></JournalIssue><Title>International journal of molecular sciences</Title><ISOAbbreviation>Int J Mol Sci</ISOAbbreviation></Journal><ArticleTitle>Autophagy Dynamics and Modulation in a Rat Model of Renal Ischemia-Reperfusion Injury.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">E7185</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.3390/ijms21197185</ELocationID><Abstract><AbstractText>Renal ischemia-reperfusion (IR) injury leading to cell death is a major cause of acute kidney injury, contributing to morbidity and mortality. Autophagy counteracts cell death by removing damaged macromolecules and organelles, making it an interesting anchor point for treatment strategies. However, autophagy is also suggested to enhance cell death when the ischemic burden is too strong. To investigate whether the role of autophagy depends on the severity of ischemic stress, we analyzed the dynamics of autophagy and apoptosis in an IR rat model with mild (45 min) or severe (60 min) renal ischemia. Following mild IR, renal injury was associated with reduced autophagy, enhanced mammalian target of rapamycin (mTOR) activity, and apoptosis. Severe IR, on the other hand, was associated with a higher autophagic activity, independent of mTOR, and without affecting apoptosis. Autophagy stimulation by trehalose injected 24 and 48 h prior to onset of severe ischemia did not reduce renal injury markers nor function, but reduced apoptosis and restored tubular dilation 7 days post reperfusion. This suggests that trehalose-dependent autophagy stimulation enhances tissue repair following an IR injury. Our data show that autophagy dynamics are strongly dependent on the severity of IR and that trehalose shows the potential to trigger autophagy-dependent repair processes following renal IR injury.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Decuypere</LastName><ForeName>Jean-Paul</ForeName><Initials>JP</Initials><Identifier Source="ORCID">0000-0001-6050-599X</Identifier><AffiliationInfo><Affiliation>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hutchinson</LastName><ForeName>Shawn</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Monbaliu</LastName><ForeName>Diethard</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martinet</LastName><ForeName>Wim</ForeName><Initials>W</Initials><Identifier Source="ORCID">0000-0003-1967-9343</Identifier><AffiliationInfo><Affiliation>Department of Pharmaceutical Sciences, University of Antwerp, B-2610 Antwerp, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pirenne</LastName><ForeName>Jacques</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jochmans</LastName><ForeName>Ina</ForeName><Initials>I</Initials><Identifier Source="ORCID">0000-0003-4592-2810</Identifier><AffiliationInfo><Affiliation>Laboratory of Abdominal Transplantation, Transplantation Research Group, Department of Microbiology and Immunology, KU Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Abdominal Transplant Surgery, University Hospitals Leuven, B-3000 Leuven, Belgium.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>KaN 1518914N</GrantID><Agency>Fonds Wetenschappelijk Onderzoek</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Int J Mol Sci</MedlineTA><NlmUniqueID>101092791</NlmUniqueID><ISSNLinking>1422-0067</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">acute kidney injury</Keyword><Keyword MajorTopicYN="N">apoptosis</Keyword><Keyword MajorTopicYN="N">autophagy</Keyword><Keyword MajorTopicYN="N">ischemia-reperfusion injury</Keyword><Keyword 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IdType="pubmed">10487768</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Belgique</li></country><region><li>Province d'Anvers</li><li>Région flamande</li></region><settlement><li>Anvers</li></settlement><orgName><li>Université d'Anvers</li></orgName></list><tree><country name="Belgique"><noRegion><name sortKey="Decuypere, Jean Paul" sort="Decuypere, Jean Paul" uniqKey="Decuypere J" first="Jean-Paul" last="Decuypere">Jean-Paul Decuypere</name></noRegion><name sortKey="Decuypere, Jean Paul" sort="Decuypere, Jean Paul" uniqKey="Decuypere J" first="Jean-Paul" last="Decuypere">Jean-Paul Decuypere</name><name sortKey="Hutchinson, Shawn" sort="Hutchinson, Shawn" uniqKey="Hutchinson S" first="Shawn" last="Hutchinson">Shawn Hutchinson</name><name sortKey="Hutchinson, Shawn" sort="Hutchinson, Shawn" uniqKey="Hutchinson S" first="Shawn" last="Hutchinson">Shawn Hutchinson</name><name sortKey="Jochmans, Ina" sort="Jochmans, Ina" uniqKey="Jochmans I" first="Ina" last="Jochmans">Ina Jochmans</name><name sortKey="Jochmans, Ina" sort="Jochmans, Ina" uniqKey="Jochmans I" first="Ina" last="Jochmans">Ina Jochmans</name><name sortKey="Martinet, Wim" sort="Martinet, Wim" uniqKey="Martinet W" first="Wim" last="Martinet">Wim Martinet</name><name sortKey="Monbaliu, Diethard" sort="Monbaliu, Diethard" uniqKey="Monbaliu D" first="Diethard" last="Monbaliu">Diethard Monbaliu</name><name sortKey="Monbaliu, Diethard" sort="Monbaliu, Diethard" uniqKey="Monbaliu D" first="Diethard" last="Monbaliu">Diethard Monbaliu</name><name sortKey="Pirenne, Jacques" sort="Pirenne, Jacques" uniqKey="Pirenne J" first="Jacques" last="Pirenne">Jacques Pirenne</name><name sortKey="Pirenne, Jacques" sort="Pirenne, Jacques" uniqKey="Pirenne J" first="Jacques" last="Pirenne">Jacques Pirenne</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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