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BH3‐only protein Bim is upregulated and mediates the apoptosis of cardiomyocytes under glucose and oxygen‐deprivation conditions
Author(s) -
Huang Chahua,
Li Juxiang,
Hong Kui,
Xia Zhen,
Xu Yan,
Cheng Xiaoshu
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10392
Subject(s) - apoptosis , gene silencing , downregulation and upregulation , microbiology and biotechnology , reactive oxygen species , cytotoxicity , ischemia , in vivo , in vitro , chemistry , mitochondrion , rna interference , cancer research , biology , medicine , biochemistry , rna , gene
Bim is a potent pro‐apoptotic BH3‐only Bcl‐2 member. However, the expression of Bim and its role in cardiac injury induced by ischemia remain unclear. H9c2 cells were subjected to a glucose and oxygen‐deprived (GOD) condition in vitro, mimicking ischemia environment in vivo. GOD treatment augmented the expression of Bim and induced the apoptosis of H9c2 cells. Silencing of Bim by RNAi significantly attenuated GOD‐induced cytotoxicity, suppressed mitochondrial membrane potential △Ψm loss, inhibited caspase 3 activation and reduced apoptosis. The data demonstrate that Bim is upregulated by GOD in a time‐dependent manner in H9c2 cells, and enhances mitochondrial apoptosis dependent on the activation of caspase 3. Silencing of Bim may be a promising therapeutic strategy in ischemia related heart diseases.