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.