CIAPIN1 promotes proliferation and migration of PDGF-BB-activated airway smooth muscle cells via the PI3K/AKT and JAK2/STAT3 signaling pathways.

Abstract

Cytokine-induced apoptosis inhibitor 1 (CIAPIN1) is an essential anti-apoptotic protein; however, its role and associated molecular pathways in asthma remain largely unexplored. This study aimed to investigate the potential effects of CIAPIN1 on the proliferation and migration of platelet-derived growth factor BB (PDGF-BB)-induced ASMCs and the underlying mechanisms involved. Considering these aspects, ASMCs are activated with PDGF-BB as a cellular model for asthma. CIAPIN1 is then downregulated using small interfering ribonucleic acid (siRNA). Western blot analysis was performed to assess protein expression. Elevated levels of CIAPIN1 were observed, demonstrating a positive correlation with cytokine levels. CIAPIN1 expression is significantly increased in PDGF-BB-induced human ASMCs. In addition, CIAPIN1 knockdown inhibited proliferation, inflammatory cytokine production, and migration ability, while elevating apoptosis in PDGF-BB-induced human ASMCs. Moreover, CIAPIN1 knockdown inhibited phosphorylated phosphoinositide 3-kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), phosphorylated Janus kinase 2 (p-JAK2), and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) protein expression. In conclusion, the results indicate that CIAPIN1 regulates the proliferation and migration of human ASMC in response to PDGF-BB by inhibiting the PI3K/AKT and JAK2/STAT3 pathways.