Mechanism of CircPTPRA Regulating ox-LDL Induced Apoptosis of Vascular Endothelial Cells Through the miR-145-5p/KLF5 Axis

This study aims to investigate the mechanism of CircPTPRA regulating ox-LDL induced apoptosis of vascular endothelial cells through the miR-145-5p/KLF5 axis. Vascular endothelial cells (EVC304) were divided into control group, ox-LDL group, ox-LDL+si-NC group, ox-LDL+si-CircPTPRA group, oxLDL+miR-NC group, ox-LDL+miR-145-5p mimic group, ox-LDL+si-CircPTPRA+inhibitor NC group, and oxLDL+si-CircPTPRA+miR-145-5p inhibitor group. The gene expression levels of CircPTPRA, miR-145-5p, and KLF5 mRNA were detected by qRT-PCR. Cell proliferation were detected by MTT and EdU staining. The levels of TNF-α, IL-6, IL-1β, MDA, SOD and GSH-Px were detected by ELISA. Cell apoptosis rate were detected by flow cytometry. Western blot was used to detect Ki-67, cleaved caspase-3 and KLF5 protein expression levels. Luciferase assay verified the relationship between miR-145-5p and CircPTPRA and KLF5. Compared with the control group, CircPTPRA and KLF5 mRNA expression levels, TNF-α, IL-6, IL-1β, MDA levels, apoptosis rate, cleaved caspase-3 and KLF5 protein levels were significantly increased in EVC-304 cells in ox-LDL group. miR-145-5p expression, cell D490 value (24, 48 h) and proliferation rate, GSH-Px and SOD levels, Ki-67 protein expression were significantly decreased. Both CircPTPRA knockout or miR-145-5p overexpression reduced cellular inflammatory response, oxidative stress and apoptosis. Compared with ox-LDL+si-CircPTPRA+inhibitor NC group, knockdown of miR-145-5p promoted cellular inflammatory response, oxidative stress and apoptosis. Interference with CircPTPRA can regulate the miR-145-5p/KLF5 axis, thereby reducing ox-LDL induced apoptosis of vascular endothelial cells.

CSTR: 32200.14.cjcb.2023.10.0002