Ca²⁺ Influx through TRPC Channels Is Regulated by Homocysteine-Copper Complexes.

ABSTRACT: An elevated level of circulating homocysteine (Hcy) has been regarded as an independent risk factor for cardiovascular disease; however, the clinical benefit of Hcy lowering-therapy is not satisfying. To explore potential unrevealed mechanisms, we investigated the roles of Ca²⁺ influx through TRPC channels and regulation by Hcy-copper complexes. Using primary cultured human aortic endothelial cells and HEK-293 T-REx cells with inducible TRPC gene expression, we found that Hcy increased the Ca²⁺ influx in vascular endothelial cells through the activation of TRPC4 and TRPC5. The activity of TRPC4 and TRPC5 was regulated by extracellular divalent copper (Cu²⁺) and Hcy. Hcy prevented channel activation by divalent copper, but monovalent copper (Cu⁺)

SUBMITTER: Chen GL 

PROVIDER: S-EPMC10296383 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature