Long-chain non-coding RNA-p21 induces apoptosis of vascular smooth muscle cells in cerebral atherosclerosis / 西安交通大学学报(医学版)

ABSTRACT

Objective: To explore the mechanism of lncRNA-p21 regulating the apoptosis of cerebral smooth muscle cells (SMCs) involved in the occurrence and development of cerebral atherosclerosis. Methods: We selected 30 subjects receiving physical checkup and 30 patients with cerebrovascular atherosclerosis in our hospital. The content of lncRNA-p21 in serum was detected by Real-time fluorescence quantitative PCR. The rat model of cerebral atherosclerosis was established. The pathological changes of rat brain were observed by HE staining. The content of lncRNA-p21 in brain tissue was detected by RT-PCR; Western blot was used to detect the expressions of mTOR, anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax. Vascular smooth muscle cells (BVSMCs) were stimulated with ox-LDL to establish atherosclerosis model of vascular SMCs. lncRNA-p21 was overexpressed or inhibited. Apoptosis was detected by flow cytometry and TUNEL. The Caspase-3 activity assay kit was used to detect the expression of Caspase-3. Western Blot was used to detect the expressions of mTOR, anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax. Results: The expression of lncRNA-p21 was significantly decreased in patients with cerebral atherosclerosis and model group rats (P<0.05). HE staining showed that the decrease of lncRNA-p21 could contribute to the pathological changes of rat brain tissue accompanied by increased activity of Caspase-3, decreased expressions of Bcl-2 and mTOR protein and increased expression of Bax protein (P<0.05). Flow cytometry and TUNEL showed that overexpression of lncRNA-p21 could reduce the apoptosis of BVSMCs, inhibiting lncRNA-p21 could promote the apoptosis of BVSMCs (P<0.05). In VSMCs, lncRNA-p21 was overexpressed, Caspase-3 activity decreased, Bcl-2, mTOR protein expression increased, and Bax protein expression decreased (P<0.05). The expression of lncRNA-p21 was inhibited; Caspase-3 activity increased; Bcl-2 and mTOR protein expressions decreased; and Bax protein expression increased (P<0.05). Conclusion: lncRNA-p21 may regulate the apoptosis of cerebrovascular smooth muscle cells by regulating the expression of mTOR protein and participate in the pathological process of cerebral atherosclerosis.