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

Figure 5.

Figure 5

miR‐145 inhibited human vascular smooth muscle cell (VSMC) proliferation in vitro. (A) Proliferation of miR‐145 inhibitor‐transduced cells from non‐atherosclerosis‐associated valvular disease (VL) patients was similar to non‐transduced cells from patients with atherosclerosis‐associated coronary heart disease (CR), and proliferation of miR‐145 mimic‐transduced cells from atherosclerosis‐associated coronary heart disease (CR) patients was similar to non‐transduced cells from patients with non‐atherosclerosis‐associated valvular disease (VL) as revealed by CCK‐8 cell counting 16 days after plating. VL/CR (nc) are cells transduced with a negative control scrambled inhibitor or mimic construct (*P < 0.05 versus VL, #P < 0.05 versus CR, n1 = 10, n2 = 4). (B) 5‐ethynyl‐2‐deoxyuridine (EdU) DNA synthesis marker (red) staining showed that the number of proliferating miR‐145 inhibitor‐transduced cells from VL donors increased to a level similar to cells from non‐transduced CR donors and the number of proliferating miR‐145 mimic‐transduced cells from CR donors increased to a level similar to cells from non‐transduced VL donors (*P < 0.05 versus VL, #P < 0.05 versus CR, n1 = 10, n2 = 4). (C) The number of miR‐145 inhibitor‐transduced VSMCs from VL donors in a proliferative phase was similar to non‐transduced VSMCs from CR donors, and the number of miR‐145 mimic‐transduced VSMCs from CR donors in a proliferative phase was similar to non‐transduced VSMCs from VL donors as shown by flow cytometry (*P < 0.05 versus VL, #P < 0.05 versus CR, n1 = 10, n2 = 4).