Key result
Down-regulation of CD36 increased the expression of p-VEGFR2 and increased proliferation of endothelial cells in hypertrophic cardiomyopathy models.
Why the study?
HCM often reveals microvascular rarefaction and myocardial ischemia, but whether CD36 affects vascular endothelial cell proliferation in HCM is unclear.
Does down-regulation of CD36 improve endothelial cell proliferation in hypertrophic cardiomyopathy models?
Does down-regulation of CD36 improve endothelial cell proliferation in hypertrophic cardiomyopathy models?
Down-regulation of CD36 increases endothelial cell proliferation via p-VEGFR2 in a mouse model of hypertrophic cardiomyopathy, suggesting a potential therapeutic target for myocardial ischemia in HCM.
CD36 modulation merits further preclinical study; leaves open any role in human hypertrophic cardiomyopathy.
Background: Hypertrophic cardiomyopathy (HCM) is a cardiovascular disease caused by genetic mutations. HCM with normal epicardial coronary arteries often reveal microvascular rarefaction and myocardial ischemia.Cluster of differentiation 36 (CD36) is a multifunctional pattern recognition membrane receptor that is highly expressed on microvascular endothelial cells (MVEC) and plays an essential role in endothelial cell function. However,whether CD36 affects vascular endothelial cell proliferation in HCM is unclear.We detected the effects of CD36 on endothelial cell proliferation and it’s underlying mechanisms in HCM. Methods: We detected the effects of CD36 on endothelial cell proliferation and it’s underlying mechanisms in HCM. These studies were complemented by in vivo analysis of CD36 expression in cTnTQ92 transgenic mice myocardium and in vitro analysis of transfection of CD36 gene or SiRNA-CD36 to endothelial cells isolated from cTnTQ92 transgenic mice heart. Results: In this study, we found that the expression of CD36 was higher and the microvessel density was lower in myocardial tissue of cTnTQ92 transgenic mice than that in the myocardial tissue of wild-type control C57BL/6 mice. The expressions of CD36 and p21 in endothelial cells isolated from cTnTQ92 transgenic mice heart were higher than those in control group. The expression levels of proliferating cell nuclear antigen (PCNA) and Cyclin D1 proteins were lower than that of control group, and the proliferation of endothelial cells was lower than that of control group, but the opposite results were obtained by transfection of SiRNA-CD36 to endothelial cells. Further studies showed that down-regulation of CD36 increased the expression of p-VEGFR2 and increased proliferation of endothelial cell. EGFR specific inhibitor AG1478 reversed these effects. Conclusions: These findings suggest down-regulation of CD36 increased the expression of p-VEGFR2 and increased proliferation of endothelial cell in hypertrophic cardiomyopathy. Down-regulation CD36 expression may be a potential therapeutic strategy for the treatment of myocardial ischemia in HCM.
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Tian et al. (2023) studied Hypertrophic cardiomyopathy. Down-regulation of CD36 vs. Control / Wild-type was evaluated on Endothelial cell proliferation (p=<0.05). Down-regulation of CD36 increased the expression of p-VEGFR2 and increased proliferation of endothelial cells in hypertrophic cardiomyopathy models.
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