Role of miR-26a/b in AngII-induced hypertensive vascular remodeling

Objective: To detect the expression of miR-26a/b in the aorta and serum of mice so as to explore the role of miR-26a/b in vascular remodeling of hypertension. Methods: C576L/BJ male mice were randomly divided into AngII group and control group. Mini-osmotic pump was implanted subcutaneously into the back of mice, and the model of blood vessel remodeling in mice was established by continuous infusion of AngII(2.0 mg/kg·d). The mice in control group were injected with saline. Blood pressure was taken before the intervention and at 3, 5, 7, 10 and 14 days after the intervention. After 2 weeks, the mice were killed, the serum and aorta tissues were collected, and the expression of miR-26a/b was determined by RT-PCR. HE staining, Masson staining and immunohistochemistry were performed to observe changes in vascular morphology, fibrosis and protein expression. Results: After the intervention, systolic blood pressure and diastolic blood pressure were significantly higher in AngII group than in control group (P<0.05). HE staining showed that the vessel wall of AngII group was thicker than that of control group. Masson staining showed more blue collagen deposition in the middle of aorta in AngII group but no obvious collagen deposition in control group. RT-PCR showed that the expression of miRNA-26a/b in the serum and aorta of AngII group was significantly lower than in control group (P<0.05). Immunohistochemistry indicated that the expressions of CTGF, collagen I and collagen III all increased after AngII infusion (P<0.05). Conclusion: MiR-26a/b, CTGF, collagen I and collagen III may be involved in AngII-induced vascular remodeling in hypertension. MiR-26a/b may be a new therapeutic target of vascular remodeling in hypertension.