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. 2016 Mar 15;20(6):1049–1061. doi: 10.1111/jcmm.12825

Figure 1.

Figure 1

miR‐145 expression and smooth muscle cell (SMC)‐specific contractile marker expression are reduced in aortas from patients with atherosclerosis‐associated cardiovascular disorders. (A) miR‐145 expression was significantly higher in aortic samples from patients with non‐atherosclerosis‐associated congenital (CN) and valvular (VL) heart disease compared to tissue from patients with atherosclerosis‐associated coronary heart disease (CR) or aortic dissection disease (AR) by RT‐qPCR (*P < 0.05 versus CN, #P < 0.05 versus VL, AR: n = 11; CR: n = 42; CN: n = 9; VL: n = 18). (B) The mRNA (by RT‐qPCR) and (C) protein expression (by Western blot) of KLF5, a target of miR‐145, was significantly decreased in CN and VL donors compared with CR and AR donors (*P < 0.05 versus CN, #P < 0.05 versus VL). (D) Immunohistochemical staining for α‐SMA (brown) to identify SMCs. Quantification showed that tissue from CN and VL patients had a significantly higher percentage of α‐SMA + cells than CR and AR samples (*P < 0.05 versus CN, #P < 0.05 versus VL). (E) Expression of α‐SMA and calponin was significantly higher in CN and VL aortas than in CR and AR aortas (*P < 0.05 versus CN, #P < 0.05 versus VL). β‐actin was used as a loading control.