Transfection of Vascular Endothelial Growth Factor B into hypertrophic cardiomyocytes promotes angiogenesis by increasing endothelial cell VEGFR1 phosphorylation levels

Abstract Background Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease characterized by the thickening of the left ventricular wall. HCM with normal epicardial coronary arteries often reveals microvascular rarefaction and myocardial ischemia. Myocardial ischemia refers to a condition in which there is inadequate blood flow to the heart muscle, resulting in a reduced oxygen supply. Vascular Endothelial Growth Factor B (VEGF-B) plays a role in angiogenesis. It promotes the proliferation and migration of endothelial cells, which are the building blocks of blood vessels. However, there is currently no specific research available on the effects and mechanisms of VEGF-B on vascular regeneration in HCM. This study aims to investigate the effects of VEGF-B on vascular regeneration in HCM. Methods This study transfected hypertrophic cardiomyocytes stimulated by Angiotensin II (Ang II) with VEGF-B and co-cultured them with human umbilical cord endothelial cells (HUVECs) to assess endothelial cell proliferation and angiogenesis to explore the role of VEGF-B in vascular regeneration in HCM. Results After co-culturing VEGF-B-transfected hypertrophic cardiomyocytes with HUVECs, we observed a significant increase in HUVEC proliferation in the VEGF-B-transfected group compared to the control group. Additionally, the tube formation ability was also enhanced in the VEGF-B-transfected group. We also found a significant increase in the expression of p-VEGFR1Y1213 in HUVECs co-cultured with VEGF-B-transfected hypertrophic cardiomyocytes compared to the control group. Conclusions In conclusion, overexpression of VEGF-B in hypertrophic cardiomyocytes can promote endothelial cell proliferation and vascular formation. This finding suggests that overexpression of VEGF-B in hypertrophic cardiomyocytes may be a potential therapeutic approach for treating myocardial ischemia in HCM.