[Potential role of microRNA-181b on atherosclerosis]

To observe the serum expression of miR-181b in atherosclerotic patients and the in vitro effects of miR-181b on vascular smooth muscle cell growth and migration.

Fifty patients (mean age: (78.1 ± 8.9) years old) with carotid ultrasound examination evidenced atherosclerotic plaque were enrolled as the atherosclerosis group and 50 healthy (mean age: (72.5 ± 10.7) years old) subjects serve as control group. Stem-loop real time RT-PCR was used to detect the serum expression of miR-181b. Importin-α3 was predicted to be a direct target of miR-181b by Targetscan and Pictar. Western-blot was employed to detect the in vitro effects of miR-181b on the expression of Importin-α3 in endothelial cells. Luciferase reporter assay was employed to testify the prediction. The effects of miR-181b on vascular smooth muscle cell growth, migration abilities were respectively examined by CCK8 assay and Matrigel migration assay.

Compared with healthy controls, serum expression of miR-181b was significantly down-regulated in patients with atherosclerosis (31.69 ± 0.96 vs. 82.28 ± 5.95, P < 0.05); Importin-α3 was predicted and proved to be a direct target of miR-181b by Western-blot and luciferase reporter assay. The proliferation and migration of vascular smooth muscle cell were significantly downregulated by forced expression of miR-181b (1.57 ± 0.18 vs. 2.66 ± 0.16, P < 0.05; 8.7 ± 1.1 vs. 21.4 ± 2.3, P < 0.05), while these effects could be abolished by inhibition of miR-181b (2.88 ± 0.09 vs. 2.04 ± 0.11, P < 0.05; 15.2 ± 1.5 vs. 8.4 ± 1.3, P < 0.05).

The serum miR-181b level was significantly reduced in patients with atherosclerosis. miR-181b may function as an atherosclerosis suppressor by interupting the NF-κB pathway in endothelial cells and inhibiting the proliferation and migration of vascular smooth muscle cells.