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- W2022381203 abstract "Stress induces cardiac dysfunction and cardiomyocyte injury, and while current data indicate that mitochondria play a key role in this process, the mechanisms remain unknown. In this study, we found that in rats, restraint stress induced nerve growth factor-induced clone B (NGFI-B) translocation from the nucleus to mitochondria in cardiomyocytes. This translocation promoted cytochrome c release from mitochondria to the cytoplasm, which ultimately resulted in cardiomyocyte apoptosis. We also found that stress induced oversecretion of glucocorticoids and activated the protein kinase A (PKA) pathway in cardiomyocytes. Enhanced PKA activity increased NGFI-B serine phosphorylation, which caused NGFI-B to translocate from the nucleus to mitochondria. Moreover, a PKA peptide inhibitor blocked NGFI-B serine phosphorylation and translocation. Our data demonstrate that stress affects cardiomyocytes by inducing NGFI-B mitochondrial translocation via serine phosphorylation, which in turn initiates mitochondrial-mediated apoptosis." @default.
- W2022381203 created "2016-06-24" @default.
- W2022381203 creator A5031953660 @default.
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- W2022381203 date "2012-01-10" @default.
- W2022381203 modified "2023-09-24" @default.
- W2022381203 title "Phosphorylated nerve growth factor-induced clone B (NGFI-B) translocates from the nucleus to mitochondria of stressed rat cardiomyocytes and induces apoptosis" @default.
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- W2022381203 doi "https://doi.org/10.3109/10253890.2011.644603" @default.
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