3.4 miR-26a inhibits VSMC proliferation in vivo and in vitro.
The development of hypertensive VR is associated with the excessive proliferation of VSMCs. To determine whether miR-26a affected VSMC proliferation, immunohistochemistry for PCNA was used to test VSMC proliferation in thoracic aortas of SHRs and WKY rats. Cells with brown staining were defined as PCNA-positive cells. The proportion of PCNA-positive cells (ratio of number of PCNA-positive cells to total number of sampled cells) was lower with rAAV-miR-26a overexpression than in vector- and vehicle-treated controls (Fig. 4a, b; 0.08801 ± 0.01623 vs 0.4440 ± 0.04262 and 0.4496 ± 0.01413, P<0.05). We used CCK‐8 assay and flow cytometry to measure the proliferation of VSMCs in vitro. Upregulation of miR‐26a reduced the proliferation of AngII-induced VSMCs and retained cells in the G1 phase (Fig. 4c-e). miR-26a inhibitor treatment had the opposite effect, promoting cell proliferation.