Zhu Ling, Zhou Jin, Gu Yunfan, Xu Yongtian, Guo Yanfang
Department of Pediatrics, Shanghai Pudong New District Gongli Hospital, Shanghai, China.
Physiol Rep. 2025 May;13(9):e70360. doi: 10.14814/phy2.70360.
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.
细胞因子诱导的凋亡抑制因子1（CIAPIN1）是一种重要的抗凋亡蛋白；然而，其在哮喘中的作用及相关分子途径仍 largely未被探索。本研究旨在探讨CIAPIN1对血小板衍生生长因子BB（PDGF - BB）诱导的气道平滑肌细胞（ASMCs）增殖和迁移的潜在影响及其潜在机制。考虑到这些方面，用PDGF - BB激活ASMCs作为哮喘的细胞模型。然后使用小干扰核糖核酸（siRNA）下调CIAPIN1。进行蛋白质印迹分析以评估蛋白质表达。观察到CIAPIN1水平升高，表明与细胞因子水平呈正相关。在PDGF - BB诱导的人ASMCs中，CIAPIN1表达显著增加。此外，CIAPIN1基因敲低抑制了PDGF - BB诱导的人ASMCs的增殖、炎性细胞因子产生和迁移能力，同时增加了细胞凋亡。此外，CIAPIN1基因敲低抑制了磷酸化磷脂酰肌醇3激酶（p - PI3K）、磷酸化蛋白激酶B（p - Akt）、磷酸化Janus激酶2（p - JAK2）和磷酸化信号转导子及转录激活子3（p - STAT3）的蛋白表达。总之，结果表明CIAPIN1通过抑制PI3K/AKT和JAK2/STAT3途径调节人ASMC对PDGF - BB的增殖和迁移反应。
