The Effect Of Zipper-Interacting Protein Kinase On High Glucose-Stimulated Human Aortic Smooth Muscle Cells

Biologic abnormalities in vascular smooth muscle cells (VSMC) may perform a crucial role in the pathogenesis of diabetic vascular disease. The principal aim of this study was to determine the effects of zipper-interacting protein kinase (ZIPK) on human aortic smooth muscle cells (HASMCs) stimulated by high glucose (HG). To elucidate the role of ZIPK in HG-treated HASMCs, we overexpressed ZIPK by lentivirus infection and knocked down ZIPK by gene deletion using ZIPK shRNA. Flow cytometry and Cell Counting kit-8 (CCK-8) were separately used to analyze cell apoptosis and proliferation. Migratory activity was examined using transwell migration chamber assays. The results showed that ZIPK overexpression inhibited cell growth and migration, enhanced cell apoptosis, and reversed cell cycle disturbance by regulating the related proteins of cellular physiological process, such as human cell division cycle 14A phosphatase (Hcdc14A) and intercellular adhesion molecule 1 (ICAM-1). In conclusion, the results suggested that ZIPK plays a role in HG-treated HASMCs, indicating ZIPK is a potential therapeutic target for the treatment of diabetic vascular complications.