ACTA2 and myocardial infarction: We examined the density of coronary arteries by using anti-cluster of differentiation 31 (CD31; also known as PECAM1; an endothelial cell marker) and α-smooth muscle actin (α-SMA; also known as ACTA2; a smooth muscle cell marker), and found that BCI treatment caused no changes in arterial angiogenesis post-MI (Fig. 2F).