miR-503/Apelin-12 mediates high glucose-induced microvascular endothelial cells injury via JNK and p38MAPK signaling pathway.

摘要: Abstract Introduction Diabetic patients are often accompanied by complications of diabetic vascular disease, which could lead to heart failure or stroke. In this work, we explored the role miR-503/Apelin-12 in angiopathy (DA) in vitro. Methods ELISA and qPCR were applied assess expression miR-503 Apelin-12 high glucose (HG)-treated microvascular endothelial cells (HMEC-1). The effects on apoptosis, inflammation oxidative stress assessed flow cytometry, western blotting, qPCR, ELISA. interaction between was evaluated dual-luciferase reporter assay, ELISA, respectively. Western blotting performed examine function JNK p38MAPK activation. Results MiR-503 markedly increased decreased HG-treated HMEC-1 cells. inhibitor significantly assuaged specifically bind 3′UTR Apelin inversely downregulate expression. Furthermore, suppressed stress. Inhibition partially reverse decrease p-JNK p-p38 levels induced suppression. Conclusion HG-induced injury, enhances regulating pathway, suggesting a potential therapeutic target for DA.