ZGLP1 Inhibits Proliferation and Migration of Smooth Muscle Cells and Promotes Apoptosis and Autophagy by Inhibiting Transforming Growth Factor Beta Receptor 1

Intracranial aneurysm is a cerebrovascular-related disease with nearly half the mortality rate and is extremely destructive. It was suggesting that human aortic smooth muscle cells play important role in intracranial aneurysm. However, the regulation of human aortic smooth muscle cells is still unclear. To explore the important regulatory role of ZGLP1 in the development and progression of human aortic smooth muscle cells, cell counting kit-8 assay and cell cloning assays were used to detect cell proliferative capacity, and flow cytometry and Transwell assays were used for apoptosis and cell migration ability, respectively. The expression of autophagy protein was examined by Western blot to explore the relationship between ZGLP1 and autophagy. In addition, the targeting relationship between ZGLP1 and transforming growth factor beta receptor 1 was verified by constructing a transforming growth factor beta receptor 1 dual luciferase recombinant plasmid. Ox-ZGLP1 and si-ZGLP1 were transfected into human aortic smooth muscle cells respectively. The Ox-ZGLP1 group had significantly lower cell clone number, proliferative capacity and migration ability than the control group. Compared with the control, ox-ZGLP1s group showed a significant increase in apoptosis rate, and the expression levels of autophagy proteins light chain 3I and light chain 3II increased by about two times. Moreover, the luciferase reporter gene activity assay confirmed the interaction of ZGLP1 on transforming growth factor beta receptor 1. After co-transfection of oe-transforming growth factor beta receptor 1 and ox-ZGLP1, the proliferation and migration ability of human aortic smooth muscle cells decreased, while apoptosis and autophagy were increased. ZGLP1 can effectively inhibit the proliferation and migration of human aortic smooth muscle cells and down-regulate the apoptosis and autophagy of human aortic smooth muscle cells by down-regulating transforming growth factor beta receptor 1 in vitro.