3.3 miR-26a ameliorates extracellular matrix (ECM) production in
vivo and in vitro.
ECM is mainly composed of collagen, so we observed and quantified CVF in
vivo by Masson’s trichrome staining. Trichrome staining and CVF were
reduced in SHRs transfected with miR-26a as compared with rAAV-GFP and
SHR-Ctrl groups (Fig. 3a, b; 31.26 ± 3.902 vs 54.25 ± 5.987 and 56.17 ±
7.218, P<0.05). Then, we transfected miR-26a mimic and
inhibitor into AngII-induced VSMCs to evaluate the effect of miR-26a on
collagen production in vitro. On qRT-PCR, miR-26a was significantly
elevated by miR-26a mimic treatment and markedly inhibited by miR-26a
inhibitor treatment in AngII-treated VSMCs; neither of their negative
controls (NCs) promoted or suppressed miR-26a expression (Fig. 3c). As
expected, miR-26a mimic overexpression significantly suppressed and
miR-26a inhibition enhanced the mRNA and protein expression of Col I and
Col III according to ELISA, qRT-PCR and western blot analysis (Fig.
3d-f). In short, miR-26a inhibited collagen deposition both in vivo and
in vitro.