Rosuvastatin and Migration of LDL-Loaded VSMC analysis by magnetic resonance imaging (MRI) of aortic and carotid artery plaques of patients treated with simvastatin have shown that statins reduced the size of the lesions and the thickness of the arterial wall without changes in the lumen size [28]. Also, recent clinical studies reported changes in carotid artery morphology in terms of increasing echogenicity and fibrous tissue content as an effect of statins [29–33]. Experimental studies using atherosclerotic animal models have suggested that the plaque-stabilizing effects of statins are related to an increase in VSMC and collagen content of the plaques [34–36]. Up to now, however, the mechanisms involved in statin-mediated enrichment and activity of VSMC in atherosclerotic plaques have not been fully characterized. In the present study, we investigated the mechanism by which rosuvastatin, a potent statin that has shown to induce stabilization of vascular lesions [31] and regression of clinical coronary atherosclerosis [27], rescues the VSMC migration kinetics and repair capacity that are impaired by accumulation of LDL. Materials and Methods Human coronary vascular SMC culture, LDL preparation, and cell treatments Primary VSMC were obtained by the explant technique from non-atherosclerotic coronary arteries of hearts, obtained from anonymized patients under heart transplantation surgery at the Figure 1. Rosuvastatin prevents the inhibitory effect of atherogenic LDL in wound repair by human VSMC. (A) Representative photomicrographs of VSMC treated without (B, D, F) or with (C, E, G) rosuvastatin in absence (B, C) or presence of nLDL (D, E), or agLDL (F, G) (B) Quantification of wound regenerated area (#: control; e: nLDL-treated cells; ¤: nLDL+rosuvastatin; %: agLDL; &: agLDL+rosuvastatin). (C) Wound regeneration kinetics (mm2/hour) of control and LDL-groups treated without/with rosuvastatin (two-way ANOVA for rosuvastatin treatment and time). Results in B and C shown as mean6SEM (n = 6 independent experiments). doi:10.1371/journal.pone.0038935.g001 PLoS ONE | www.plosone.org 2 June 2012 | Volume 7 | Issue 6 | e38935