Silencing ARNTL in human carotid SMCs inhibits proliferation and induces cellular senescence. Human carotid SMCs were treated with siRNA against ARNTL followed by functional assays. SMCs were also treated with or without PDGF-BB after ARNTL silencing and ARNTL gene expression levels were measured (A). (B) Proliferation was measured as a function of cell confluence using Incucyte Zoom system (Essen BioScience) (n = 4). (C) Gene expression levels of contractile SMC markers were measured using qRT-PCR (n = 4) and (D) protein levels of contractile protein α-SMA (42 kDa). Protein levels were quantified using immunoblots from 3 experiments and representative blots are shown. ACTA2, α-SMA; CNN1, calponin1; MYH11, myosin heavy chain-11; LMOD1, leiomodin1; SMTN, smoothelin; α-SMA. Data points are represented as mean ± SEM. Statistical differences were calculated using student t-test. *P < .05, **P < .01, ***P < .001