3.2 miR-26a had a protective effect on hypertensive VR
To evaluate the role of miR-26a in hypertensive VR, rAAV vectors were constructed to overexpress miR-26a in SHRs. As expected, rAAV-miR-26a transfection significantly increased the expression of miR-26a in aortas and plasma of SHRs (Fig. 2a). Meanwhile, rAAV-miR-26a prevented systolic blood pressure (SBP) from continuously increasing in SHRs (Supplemental Fig. S1). To evaluate VR, thoracic aortas underwent H&E staining. As compared with normal WKYs, in SHRs, the media of the thoracic aorta was significantly thickened. However, miR-26a overexpression could reduce the medial thickening of the thoracic aorta caused by hypertension. The MT/LD ratio declined profoundly with miR-26a overexpression (Fig. 2b, c; rAAV-miR-26a vs rAAV-GFP and SHR-Ctrl was 5.430 ± 0.2943 vs 6.793 ± 0.4130 and 7.575 ± 1.584; P<0.05). Immunohistochemistry for smooth muscle α-actin showed well-distributed smooth muscle and intact intima in WKY rats. However, VSMCs formed intima hyperplasia and parts of the vascular walls protruded into the aortic lumen in the SHR-Ctrl and rAAV-GFP groups. rAAV-miR-26a treatment significantly improved smooth muscle alignment and integrity (Fig. 2b).