Recent studies have identified low levels of myocyte apoptosis (80-250 myocytes per 10 5 nuclei) in failing human hearts. It remains unclear, however, whether this cell death is a coincidental finding, a protective process, or a causal component in pathogenesis.
Interestingly, although 8-Br-cAMP markedly induced apoptosis in cardiac myocytes, it completely blocked serum depletion-induced apoptosis in PC12 cells, a rat pheochromocytoma cell line.
Stimulation of 1-AR, but not 2-AR, markedly induced myocyte apoptosis, as indicated by increased terminal deoxynucleotidyltransferase-mediated UTP end labeling or Hoechst staining positive cells and DNA fragmentation.
Such details provide a deeper understanding and appreciation for Markedly Induced Myocyte Apoptosis.
...downregulating OTUD1 in MI/R induced myocyte apoptosis.
This particular example perfectly highlights why Markedly Induced Myocyte Apoptosis is so captivating.
Figure 6. Saturated FA-induced apoptosis in cardiac myocytes with loss of SCD1 function using siRNA transfection. Cardiac myocytes were transfected with siGFP as a control or siSCD1 at 20 mM, and simultaneously treated with palmitic acid (PA) or stearic acid (SA).
Blocking the L-type Ca2+ channel, buffering intracellular Ca2+, or inhibiting CaMKII activity fully protects cardiac myocytes against 1AR-induced apoptosis, and overexpressing a cardiac CaMKII isoform, CaMKII-C, markedly exaggerates the 1AR apoptotic effect.
