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[1]李丽敏,孙卫星.TRIM22 抑制PDGF-BB诱导的气道平滑肌细胞的炎症、增殖和迁移[J].天津医科大学学报,2025,31(04):358-363.[doi:10.20135/j.issn.1006-8147.2025.04.0358]
 LI Limin,SUN Weixing.TRIM22 inhibits inflammation, proliferation, and migration of PDGF-induced airway smooth muscle cells[J].Journal of Tianjin Medical University,2025,31(04):358-363.[doi:10.20135/j.issn.1006-8147.2025.04.0358]
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TRIM22 抑制PDGF-BB诱导的气道平滑肌细胞的炎症、增殖和迁移(PDF)

《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
31卷
期数:
2025年04期
页码:
358-363
栏目:
基础医学
出版日期:
2025-07-10

文章信息/Info

Title:
TRIM22 inhibits inflammation, proliferation, and migration of PDGF-induced airway smooth muscle cells
文章编号:
1006-8147(2025)04-0358-06
作者:
李丽敏1孙卫星2
(义马煤业集团股份有限公司总医院1.呼吸与危重症医学科;2.儿科,义马 472300)
Author(s):
LI Limin1 SUN Weixing2
(1.Department of Respiratory and Critical Care Medicine,Yima Coal Industry Group Company General Hospital,Yima 472300,China;2.Department of Pediatrics,Yima Coal Industry Group Company General Hospital,Yima 472300,China)
关键词:
哮喘TRIM22PDGF-BB气道平滑肌细胞PI3K/Akt
Keywords:
asthma TRIM22 PDGF-BB airway smooth muscle cells PI3K/Akt
分类号:
R56
DOI:
10.20135/j.issn.1006-8147.2025.04.0358
文献标志码:
A
摘要:
目的:探讨 TRIM22 在气道平滑肌细胞(ASMCs)功能中的作用。方法:以血小板衍生生长因子(PDGF)-BB诱导的ASMCs为哮喘细胞模型,采用qPCR和免疫印迹检测TRIM22表达,利用CCK-8、Transwell及伤口愈合实验评估细胞增殖与迁移能力,采用ELISA和免疫印迹法检测炎症,并通过免疫印迹验证其作用机制。结果:TRIM22在PDGF-BB诱导的ASMCs中表达水平降低(t=19.57,P<0.001);PDGF-BB处理组ASMCs的细胞活力显著提高(P<0.01),而TRIM22过表达显著抑制了PDGF-BB引起的细胞生长能力增强(t=7.93,P<0.01),同时显著抑制PDGF-BB引起的迁移能力提升(t=7.95,P<0.001)。TRIM22过表达能够显著抑制PDGF-BB诱导的炎症因子[肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6]分泌(TNF-α:t=5.57,P<0.01;IL-1β:t=5.53,P<0.01;IL-6:t=7.42,P<0.01)。此外,免疫印迹实验结果表明,PDGF-BB诱导的ASMCs中核因子(NF)-κB的磷酸化水平显著升高,而TRIM22过表达显著降低了NF-κB的磷酸化水平(t=9.51,P<0.01)。同时,TRIM22抑制了PDGF-BB诱导的ASMCs中磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)信号通路的激活,表现为抑制PDGF-BB诱导的PI3K和Akt的磷酸化水平(PI3K:t=5.61,P<0.01;Akt:t=3.56,P<0.01)。结论:TRIM22通过PI3K/Akt信号通路抑制PDGF-BB引起的ASMCs的炎症、增殖及迁移。
Abstract:
Objective: To investigate the role of TRIM22 in the function of airway smooth muscle cells(ASMCs). Methods: Platelet-derived growth factor (PDGF)-BB induced ASMCs were used as a cellular model of asthma. The expression of TRIM22 was detected using qPCR and immunoblotting. Cell proliferation and migration were assessed using CCK-8, Transwell, and wound-healing assays. Inflammatory responses were evaluated by ELISA and Western blotting. The mechanism of action was further validated through Western blotting. Results: The expression level of TRIM22 in PDGF-BB was induced ASMCs decreased (t=19.57,P<0.001). In the PDGF-BB treatment group, the cell viability of ASMCs was significantly increased (P<0.01), while the overexpression of TRIM22 significantly inhibited the enhancement of cell growth induced by PDGF-BB(t=7.93,P<0.01) and the enhancement of migration induced by PDGF-BB (t=7.95,P<0.001). Overexpression of TRIM22 could significantly inhibit the secretion of PDGF-BB induced inflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-1 β, and IL-6 (TNF-α:t=5.57,P<0.01;IL-1β:t=5.53,P<0.01;IL-6:t=7.42,P<0.01). In addition, Western blotting showed that the phosphorylation level of nuclear factor (NF)-κB in ASMCs induced by PDGF-BB was significantly increased, while overexpression of TRIM22 significantly decreased the phosphorylation level of NF-κB(t=9.51,P<0.01). Meanwhile, TRIM22 inhibited the activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway in ASMCs induced by PDGF-BB, and inhibited the phosphorylation levels of PI3K and Akt induced by PDGF-BB(PI3K:t=5.61,P<0.01; Akt:t=3.56,P<0.01). Conclusion: TRIM22 suppresses inflammation, proliferation, and migration of PDGF-BB induced ASMCs through the PI3K/Akt pathway.

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备注/Memo

备注/Memo:
作者简介 李丽敏(1981-),女,学士,副主任医师,研究方向:呼吸与危重症;通信作者:孙卫星,E-mail:15239886278@163.com。
更新日期/Last Update: 2025-07-10