Zinc finger GATA-like protein 1 regulates apoptosis and phenotypic transformation via protein kinase B pathway in human vascular smooth muscle cells

Purpose Intracranial aneurysms represent the primary source of subarachnoid hemorrhage, ranking as the third most common cerebrovascular disorder after cerebral thrombosis and hypertension-related brain hemorrhage. As a member of the GATA family transcription factors, the role of zinc finger GATA-like protein 1 (ZGLP1) was unclear in intracranial aneurysm. In the present research, the specific effects of ZGLP1 on the proliferation and phenotypic transformation of human aerobic smooth muscle cells (HASMCs) were investigated. Methods Cell counting kit 8 and colony formation assays were performed to detect the growth of HASMCs. Cell migration was confirmed using transwell and wound healing assays. The apoptosis was analyzed using flow cytometry. Finding ZGLP1 knockdown inhibited the viability and colony formation ability of HASMCs. Importantly, ZGLP1 knockdown effectively promoted the apoptosis of HASMCs. The migration of HASMCs was remarkably inhibited by ZGLP1-specific small interfering RNA. Mechanistically, ZGLP1 knockdown inhibits the phosphorylation of protein kinase B (AKT) and cyclin D1 expression. In addition, ZGLP1 knockdown inhibited the expression of SMA and SM22α, while promoting the expression of OPN and MMP-2 in HASMCs, suggesting that ZGLP1 knockdown initiated the transformation from contractile phenotype to synthetic phenotype of HASMCs. Conclusion ZGLP1 knockdown induces apoptosis through the AKT pathway, and also induces the phenotypic transformation of HASMCs. ZGLP1 is a potential therapeutic target for intracranial aneurysm and deserves further research.