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dc.contributor.authorLi, Hongzhu
dc.contributor.authorZhang, Chao
dc.contributor.authorSun, Weiming
dc.contributor.authorLi, Lina
dc.contributor.authorWu, Bo
dc.contributor.authorBai, Shuzhi
dc.contributor.authorLi, Hongxia
dc.contributor.authorZhong, Xin
dc.contributor.authorWang, Rui
dc.contributor.authorWu, Lingyun
dc.contributor.authorXu, Changqing
dc.date.accessioned2015-09-01T16:59:09Z
dc.date.available2015-09-01T16:59:09Z
dc.date.issued2015-07-30
dc.identifier.citationCell & Bioscience. 2015 Jul 30;5(1):43
dc.identifier.urihttp://dx.doi.org/10.1186/s13578-015-0035-9
dc.identifier.urihttp://hdl.handle.net/10724/31697
dc.description.abstractAbstract The physiological and pathological roles of hydrogen sulfide (H2S) in the regulation of cardiovascular functions have been recognized. H2S protects against the hypoxia/reoxygenation (H/R)-induced injury and apoptosis of cardiomyocytes, and ischemic post-conditioning (PC) plays an important role in cardioprotection from H/R injury in neonatal cardiomyocytes but not in aging cardiomyocytes. Whether H2S is involved in the recovery of PC-induced cardioprotection in aging cardiomyocytes is unclear. In the present study, we found that both H/R and PC decreased cystathionine-γ-lyase (CSE) expression and the production rate of H2S. Supplementation of NaHS protected against H/R-induced apoptosis, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome c (Cyt c), and mPTP opening. The addition of NaHS also counteracted the reduction of cell viability caused by H/R and increased the phosphorylation of ERK1/2, PI3K, Akt, GSK-3β and mitochondrial membrane potential. Additionally, NaHS increased Bcl-2 expression, promoted PKC-ε translocation to the cell membrane, and activated mitochondrial ATP-sensitive K channels (mitoKATP). PC alone did not provide cardioprotection in H/R-treated aging cardiomyocytes, which was significantly restored by the supplementation of NaHS. In conclusion, our results suggest that exogenous H2S restores PC-induced cardioprotection via the inhibition of mPTP opening by the activation of the ERK1/2-GSK-3β, PI3K-Akt-GSK-3β and PKC-ε-mitoKATP pathways in aging cardiomyocytes. These findings provide a novel target for the treatment of aging ischemic cardiomyopathy.
dc.titleExogenous hydrogen sulfide restores cardioprotection of ischemic post-conditioning via inhibition of mPTP opening in the aging cardiomyocytes
dc.typeJournal Article
dc.date.updated2015-07-29T18:13:03Z
dc.language.rfc3066en
dc.rights.holderLi et al.


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