Role of Mydgf in the regulation of hypoxia/reoxygenation-induced apoptosis in cardiac microvascular endothelial cells

We aimed to explore the effects of myeloid-derived growth factor (Mydgf) on the regulation of hypoxia/reoxygenation (HR)-induced apoptosis of cardiac microvascular endothelial cells (CMECs). CMECs were exposed to hypoxia for 24 h and reoxygenation for 6 h to establish an HR cell model. Subsequently, an adenovirus was used to overexpress Mydgf in CMECs. Flow cytometry and TUNEL staining were used to detect the extent of apoptosis, whereas qPCR was used to detect the relative expression of Mydgf mRNA. Western blotting was also performed to detect the expression of apoptosis-related proteins and endoplasmic reticulum stress (ERS)-related proteins, including C/EBP Homologous Protein (CHOP), glucose-regulated protein 78 (GRP 78), and cleaved Caspase-12. The endoplasmic reticulum stress agonist tunicamycin (TM) was used to stimulate CMECs for 24 h as a rescue experiment for Mydgf. Flow cytometry revealed that the HR model effectively induced endothelial cell apoptosis, whereas qPCR and western blotting showed that Mydgf mRNA and protein levels decreased significantly after HR treatment (P < 0.05). Overexpression of Mydgf in cells effectively reduced apoptosis after HR. Furthermore, western blotting showed that HR induced a significant upregulation of CHOP, GRP78, and cleaved-Caspase-12 expression in CMECs, whereas HR-treated cells downregulated the expression of CHOP, GRP78, and cleaved-Caspase-12 after Mydgf overexpression. Under HR conditions, TM significantly reversed the protective effect of Mydgf on CMECs. Mydgf may reduce CMEC apoptosis induced by HR by regulating oxidative stress in ERS.

Automated summary

Mydgf can reduce apoptosis of cardiac microvascular endothelial cells (CMECs) induced by hypoxia/reoxygenation (HR) through regulating oxidative stress in endoplasmic reticulum stress (ERS).