Abstract
Enhanced apoptosis of cardiomyocytes in suffering overloaded saturated fatty acids (SFAs) can result in myocardial infarction and cardiac dysfunction. The function of vascular endothelial growth factor (VEGF) in cardiomyocyte protection was not clearly described. To investigate the preservative effects of VEGF sensitization on ceramide-mediated programmed cell death of cardiomyocytes, palmitate-induced injury in H9c2 cells was established as an in vitro model. Results revealed that 0.5 mM palmitate application effectively led to debased viability and activated apoptotic factors. A significant time-dependent relation between PAL and cardiomyocyte injury was observed. The apoptosis rate was increased greatly after 16 h of treatment with 0.5 mM PAL. In addition, cell viability was restored by VEGF overexpression during treatment with 0.5 mM PAL. Reduced apoptosis rate and expression of caspase 3, Bax, and NF-κB p65 were observed in this process, while boosted Bcl-2, p-JNK/JNK expression and activity of caspase 3 were checked. However, p-ERK/ERK levels did not exhibit a significant change. These findings indicated the protective effects of VEGF in confronting the ceramide-induced cardiomyocyte apoptosis, and would devote therapeutic targets for cardiovascular safeguard in dealing with fatty acid stress.
Highlights
Recent studies support the hypothesis that cardiomyocytes harbor no ability of self-renewal and replication, for they are terminally differentiated cells (Heallen et al 2019)
Transgenic mouse models with abnormal lipid accumulation in the heart demonstrated that an imbalance of lipid uptake and utilization in cardiomyocytes led to apoptosis and contributed to cardiomyopathy (Cheng et al 2004; Chiu et al 2005)
Effects of different PAL concentrations on cell survival and apoptosis To determine the suitable concentration of palmitate (PAL) in inducing cardiomyocyte cell injury model, H9c2 cells were treated with PAL at final concentrations of 0.2, 0.5, 0.8, and 1.2 mM and collected after 24 h to measure cell viability
Summary
Recent studies support the hypothesis that cardiomyocytes harbor no ability of self-renewal and replication, for they are terminally differentiated cells (Heallen et al 2019). The rapid changes in the human diet, and the concomitant increase in human fat deposition, have led to a high incidence of obesity, diabetes, and cardiovascular diseases (Li et al 2020). Increases in serum lipid levels result in damage to and irritation of the cardiovascular system; ectopic fat deposition places an additional burden on the Palmitate (PAL), a saturated fatty acid, has been shown to accumulate in cardiomyocytes, vascular smooth muscle cells, hepatic cells, and islet beta cells (Chai and Liu 2007; Quan et al 2014; Gorgani-Firuzjaee et al 2014; Le et al 2020; Geng et al 2020). PAL was found to induce apoptosis in a variety of cells in vitro; the exact molecular and cellular mechanisms by which fatty acids cause apoptosis remain unclear
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