Key result
Renin-b overexpression in H9c2 cells mediates cardioprotective effects under anoxia by reducing mitochondrial-induced apoptosis angiotensin-independently and caspase-induced apoptosis angiotensin-dependently.
Why the study?
Renin transcripts encoding a cytoplasmic isoform, renin-b, are not harmful and may be protective, unlike classic activated RAS.
Does renin-b overexpression prevent apoptosis and necrosis in H9c2 cells after anoxia?
Does renin-b overexpression prevent apoptosis and necrosis in H9c2 cells after anoxia?
Renin-b overexpression provides cardioprotective effects against anoxia-induced apoptosis in H9c2 cells through both angiotensin-dependent and independent pathways.
Renin-b depletion may worsen cardiomyocyte injury; hypothesis-generating for its protective role in human cardiac disease.
The renin-angiotensin system is known to regulate blood pressure as well as water- and electrolyte balance. An activated RAS is involved in the development of hypertension and hypertension-related organ damage. Thus, inhibitors of the RAS are protective and markedly increasing the life span of patients. In contrast, renin transcripts have been discovered encoding a cytoplasmatic renin isoform, termed renin-b, which is not harmful but may be even protective. Here we demonstrate that depletion of renin-b encoding transcripts by small interference RNA decreased ATP levels and increased basal necrosis as well as apoptosis rates. Furthermore, renin-b depletion potentiated the anoxia-induced increase of necrosis rates. Vice versa, overexpression of renin-b prevented the anoxia-induced increase of caspase-mediated apoptosis rates. Besides, cells overexpressing renin-b exhibited even reduced mitochondrial mediated apoptosis rates under anoxia, when compared with normoxic conditions, as indicated by Annexin V labeling. However, whereas the protective effect of renin-b on caspase-mediated apoptosis was completely blocked by the renin inhibitor CH732, the effect on mitochondrial-mediated apoptosis was not affected by CH732 at all. From these data we conclude that renin-b overexpression mediates cardioprotective effects under anoxia with respect to mitochondrial induced apoptosis angiotensin-independently, but with respect to caspase induced apoptosis likely in an angiotensin-dependent manner.
No takes yet. Share an insight, caveat, or question.
Wanka et al. (2020) studied Anoxia-induced cell death. Renin-b overexpression or siRNA depletion vs. Empty vector (pIRES) or scrambled siRNA was evaluated on Necrosis and apoptosis rates. Renin-b overexpression in H9c2 cells mediates cardioprotective effects under anoxia by reducing mitochondrial-induced apoptosis angiotensin-independently and caspase-induced apoptosis angiotensin-dependently.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:
More from Scientific Reports