Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury

PUTTA, PRIYA; BIRNBAUMER, LUTZ; DRISCOLL, ERIN C.; ROSENBAUM, MICHAEL A.; SMITH, ANDREW H.; CHAUDHURI, PINAKI; GRAHAM, LINDA M.

JVS: Vascular Science

JVS: Vascular Science

Año: 2020 vol. 1 p. 136 - 150

2666-3503

Previous studies showed the benefit of canonical transient receptor potential 6 (TRPC6) channel deficiency in promoting endothelial healing of arterial injuries in hypercholesterolemic animals. Long-term studies utilizing a carotid wire-injury model were undertaken in wild-type (WT) and TRPC6-/- mice to determine the effects of TRPC6 on phenotypic modulation of vascular smooth muscle cells (SMC) and neointimal hyperplasia. We hypothesized that TRPC6 was essential in the maintenance or reexpression of a differentiated SMC phenotype and minimized luminal stenosis following arterial injury.