The loss of CARMN regulates vascular smooth muscle cell phenotype and accelerates the development of atherosclerosis in mice.

We investigated the function of CARMN lncRNA, located immediately upstream of the miRNAs miR-143 and miR-145, as critical regulator of vSMC phenotypes in vitro and the consequence of its loss during the development of atherosclerosis in vivo. We hypothesized that loss of CARMN is a primary event controlling the functional switch towards pro-atherogenic vSMC phenotypes and accelerates the development of the plaques in vivo. RNA sequencing was performed on primary Human Coronary Arterial Smooth Muscle Cells (HCASMCs), under basal (0.2%FBS) or stimulated with PDGF-ββ (20 ng/mL), scratch stimulus or loaded with methyl-β-cyclodextrin (MBCD) (10ng/ml) exposed to either CARMN depletion via GapmeR (GapCARMN) or GapmeR control (GapCTR). Each treatment was done in triplicates.