Semaphorin 7A promotes human vascular smooth muscle cell proliferation and migration through the β-catenin signaling pathway

Background: Vascular smooth muscle cells (VSMCs) undergo a conversion from contractile phenotype to proliferative synthetic phenotype, contributing the pathogenesis of cardiovascular diseases. Semaphorin 7A (SEMA7A) is glycosylphosphatidylinositol-anchored membrane protein that plays an important role in vascular homeostasis by regulating endothelial cell behaviors. However, expression and SEMA7A VSMCs remain unclear.Methods: In this study, we screened for VSMC-regulating genes publicly available datasets analyzed human coronary artery (hCASMCs) treated with platelet-derived growth factor-BB (PDGF-BB). The effects overexpression knockdown on hCASMC proliferation migration were examined. signaling pathways involved action hCASMCs determined.Results: Bioinformatic analysis showed was significantly dysregulated oxidized low-density lipoprotein or overexpressing progerin, pro-atherogenic gene. PDGF-BB stimulation led concentration- time-dependent induction SEMA7A. Depletion attenuated PDGF-BB-induced migration. Conversely, enhanced Mechanistically, stimulated activation β-catenin pathway upregulated c-Myc, CCND1, MMP7. Knockdown impaired SEMA7A-induced migration.Conclusions: triggers switching through may serve as potential therapeutic target