Transient receptor potential canonical 3/5 attenuate endothelial damage-induced neointima formation without affecting endothelial cell proliferation.

Store-operated calcium channels (SOCCs) are involved in the process of cell proliferation; however, their expression levels differ among cell types and information on their effects in different cells is lacking. This study aimed to compare the differing effects of SOCCs on the proliferation of vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs), and the repair ability of SOCC after vascular endothelial injury. Rat primary coronary VSMCs and VECs were cultured in vitro and expression levels of SOCC molecules were detected by western blotting and quantitative polymerase chain reaction. Various molecules were selected and transfected into VSMCs and VECs using an adenovirus vector, and cell proliferation, the cell cycle, and intracellular Ca2+ were then detected. We also established a rat carotid artery endothelial injury model to verify the results of the in vitro experiments. Expression levels of transient receptor potential canonical (TRPC) 3 and TRPC5 were higher in VSMCs than in VECs. Silencing TRPC3/5 significantly inhibited cell proliferation and Ca2+ influx in VSMCs, but not in VECs. Silencing TRPC3/5 after rat carotid artery endothelial injury inhibited neointima formation, with a better reparative effect on the endothelial cell layer than rapamycin. TRPC3/5 participates in the proliferation of VSMCs via SOCCs, and silencing its expression inhibits the formation of neointima after endothelial injury. However, this effect was not significant in VECs, suggesting that other compensatory pathways may have emerged.