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Article: Caveolin-3 Peptide Protects Cardiomyocytes from Apoptotic Cell Death via Preserving Superoxide Dismutase Activity and Inhibiting Caspase-3 Activation under Hypoxia-reoxygenation
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TitleCaveolin-3 Peptide Protects Cardiomyocytes from Apoptotic Cell Death via Preserving Superoxide Dismutase Activity and Inhibiting Caspase-3 Activation under Hypoxia-reoxygenation
 
AuthorsShen, J
Lee, WS
Chen, J
Yang, D
 
KeywordsCaveolins
Oxidative stress
Cardiomyocytes
Hypoxia-reoxygenation
Apoptosis
 
Issue Date2011
 
PublisherNew World Publishing International. The Journal's web site is located at http://www.nwpii.com/ajbms.htm
 
CitationAmerican Journal of Biomedical Sciences, 2011, v. 3 n. 2, p. 126-144 [How to Cite?]
DOI: http://dx.doi.org/10.5099/aj110200126
 
AbstractRecent progress suggests that caveolins are cardiac protective molecules in regulating apoptotic cell death during myocardial ischemia-reperfusion injury. To understand the mechanisms of caveolins in cardiac protection, we investigated the expressions of caveolin-1(cav-1), caveolin-2 (cav-2) and caveolin-3 (cav-3) proteins in the isolated cultured hypoxia-reoxygenated cardiomyocytes. Neonatal rat cardiomyocytes were subjected to 4 h hypoxia and 24 h reoxygenation by exposed to 1% [O2] and replaced with normal air respectively. The expression of cav-3, instead of cav-1 and cav-2, was down-regulated by hypoxia-reoxygenation. Pre-treatments of superoxide dismutase and catalase (SOD/CAT) or peroxynitrite decomposition catalyst FeTMPyP prevented the down-regulation of cav-3. We then investigated the effects of extraneous free radicals on regulating the expression of cav-3 by incubating with xanthine/xanthine oxidase (X/XO), H2O2, 1-[N, N-di-(2-aminoethyl) amino] diazen-1-ium-1, 2-diolate (DETA/NO, NO donor) or 3-morpholinosydnonimine (SIN-1, peroxynitrite donor) respectively. Treatments of X/XO, H2O2, DETA/NO and SIN-1 significantly induced the down-regulation of cav-3 protein. The results indicate that the productions of free radicals contribute to the down-regulation of cav-3 protein in the hypoxia-reoxgenated cardiomyocytes. Moreover, our data showed that cav-3 peptide significantly enhanced the expression and the activity of SOD, inhibited O2.- production and caspase 3 activity, and reduced the rates of early and late apoptotic cell death, whereas cav-1 peptide had no effect on SOD, but slightly reduced O2.- production and decreased the rates of apoptotic cell death in the hypoxia-reoxygenated cardiomyocytes. Taken together, we conclude that caveolin-1 and caveolin-3 could ameliorate free radicals-induced oxidative injury via diverse mechanisms in hypoxia-reoxygenated cardiomyocytes.
 
DescriptionOpen Access Journal
 
ISSN1937-9080
 
DOIhttp://dx.doi.org/10.5099/aj110200126
 
DC FieldValue
dc.contributor.authorShen, J
 
dc.contributor.authorLee, WS
 
dc.contributor.authorChen, J
 
dc.contributor.authorYang, D
 
dc.date.accessioned2011-08-26T14:41:03Z
 
dc.date.available2011-08-26T14:41:03Z
 
dc.date.issued2011
 
dc.description.abstractRecent progress suggests that caveolins are cardiac protective molecules in regulating apoptotic cell death during myocardial ischemia-reperfusion injury. To understand the mechanisms of caveolins in cardiac protection, we investigated the expressions of caveolin-1(cav-1), caveolin-2 (cav-2) and caveolin-3 (cav-3) proteins in the isolated cultured hypoxia-reoxygenated cardiomyocytes. Neonatal rat cardiomyocytes were subjected to 4 h hypoxia and 24 h reoxygenation by exposed to 1% [O2] and replaced with normal air respectively. The expression of cav-3, instead of cav-1 and cav-2, was down-regulated by hypoxia-reoxygenation. Pre-treatments of superoxide dismutase and catalase (SOD/CAT) or peroxynitrite decomposition catalyst FeTMPyP prevented the down-regulation of cav-3. We then investigated the effects of extraneous free radicals on regulating the expression of cav-3 by incubating with xanthine/xanthine oxidase (X/XO), H2O2, 1-[N, N-di-(2-aminoethyl) amino] diazen-1-ium-1, 2-diolate (DETA/NO, NO donor) or 3-morpholinosydnonimine (SIN-1, peroxynitrite donor) respectively. Treatments of X/XO, H2O2, DETA/NO and SIN-1 significantly induced the down-regulation of cav-3 protein. The results indicate that the productions of free radicals contribute to the down-regulation of cav-3 protein in the hypoxia-reoxgenated cardiomyocytes. Moreover, our data showed that cav-3 peptide significantly enhanced the expression and the activity of SOD, inhibited O2.- production and caspase 3 activity, and reduced the rates of early and late apoptotic cell death, whereas cav-1 peptide had no effect on SOD, but slightly reduced O2.- production and decreased the rates of apoptotic cell death in the hypoxia-reoxygenated cardiomyocytes. Taken together, we conclude that caveolin-1 and caveolin-3 could ameliorate free radicals-induced oxidative injury via diverse mechanisms in hypoxia-reoxygenated cardiomyocytes.
 
dc.description.naturelink_to_OA_fulltext
 
dc.descriptionOpen Access Journal
 
dc.identifier.citationAmerican Journal of Biomedical Sciences, 2011, v. 3 n. 2, p. 126-144 [How to Cite?]
DOI: http://dx.doi.org/10.5099/aj110200126
 
dc.identifier.doihttp://dx.doi.org/10.5099/aj110200126
 
dc.identifier.epage144
 
dc.identifier.hkuros189750
 
dc.identifier.issn1937-9080
 
dc.identifier.issue2
 
dc.identifier.spage126
 
dc.identifier.urihttp://hdl.handle.net/10722/138121
 
dc.identifier.volume3
 
dc.languageeng
 
dc.publisherNew World Publishing International. The Journal's web site is located at http://www.nwpii.com/ajbms.htm
 
dc.publisher.placeUnited States
 
dc.relation.ispartofAmerican Journal of Biomedical Sciences
 
dc.subjectCaveolins
 
dc.subjectOxidative stress
 
dc.subjectCardiomyocytes
 
dc.subjectHypoxia-reoxygenation
 
dc.subjectApoptosis
 
dc.titleCaveolin-3 Peptide Protects Cardiomyocytes from Apoptotic Cell Death via Preserving Superoxide Dismutase Activity and Inhibiting Caspase-3 Activation under Hypoxia-reoxygenation
 
dc.typeArticle
 
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