Nucleostemin exerts anti-apoptotic function via p53 signaling pathway in cardiomyocytes

Abstract

Cardiomyocytes apoptosis following reperfusion injury causes irreversible damage to cardiac function. Understanding the mechanisms underlying cardiomyocytes death under these conditions can be helpful to identify strategies to abrogate such detrimental effects. Stem cell-specific proteins and regulatory pathways become important in understanding reparative processes in the myocardium. One such regulatory protein named nucleostemin (NS) has vital roles in cardiac ischemia. Although the relationship between NS and cell apoptosis has been studied, it is unknown how NS is controlled and how it participates in cardiomyocytes apoptosis induced by ischemia reperfusion (I/R). In the present study, we aimed to investigate the direct role of NS in myocardial I/R. In vivo, NS was highly expressed in cardiac tissues after I/R. Double immunofluorescent staining showed that NS located in the nucleolar of cardiomyocytes and correlated with cardiomyocytes apoptosis. Furthermore, in vitro primary rat cardiomyocytes increased NS expression induced by hypoxia-reoxygenation (H/R) treatment, in line with results in vivo. Suppression of NS expression by siNS promoted the expression of terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL)-positive cells p53 and cleaved caspase-3, which demonstrates I/R may require increased expression of NS to suppress p53 activation and maintain cardiomyocytes survival.

Expression profile analysis of lncRNA and mRNA in uterosacral ligaments of women with pelvic organ prolapse by RNA-seq

“…[ 37 ] Research has shown that hypoxia may require increased apoptosis of cardiomyocytes via the activated p53 signaling pathway. [ 38 ] The previous study of our research group showed that expression levels of HIF-1α and apoptosis cells were significantly increased in the POP group. [ 39 ] Therefore, HIF-1α may promote fibroblast apoptosis by activating the p53 signaling pathway, and then reducing the production of collagen.…”

CircRNA8220 Sponges MiR-8516 to Regulate Cell Viability and Milk Synthesis via Ras/MEK/ERK and PI3K/AKT/mTOR Pathways in Goat Mammary Epithelial Cells

“…Bcl-2 inhibits the activation of the upstream caspase protease by interfering with release of cytochrome c, result in inhibition cell apoptpsis [ 30 ]. As a composition of the ion channel on the mitochondrial membrane, Bax protein allows cytochrome c to pass through the mitochondrial membrane, activating caspase-9 further activating caspase-3, thus resulting in cell apoptosis [ 31 ]. Procaspase-9, an initiator caspase in the mitochondrial pathway, is recruited and activated by the apoptosome leading to downstream casepase-3 processing [ 32 ].…”

Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway

“…Bcl-2 blocks the activation of the upstream caspase protease by interfering with the release of cytochrome c, thus inhibiting cell apoptosis (24). As a composition of the ion channel on the mitochondrial membrane, Bax protein allows cytochrome c to pass through the mitochondrial membrane, activating caspase-9, and further activating caspase-3, thus resulting in cell apoptosis (9). The results revealed that si-caspase-2 also reduced the effects of iodine-131-reduced cell proliferation and induced apoptosis in human cardiac muscle cells through the t-BID/cytochrome c/ caspase-3 signaling pathway.…”

“…Bcl-2 gene expression can block the p53-induced cell apoptosis, which is independent of changes in p53 expression and its location in the nucleus; in addition, it can inhibit the bax transcription of p53 (7,8). Bcl-2 is an important anti-apoptotic factor (9).…”