武汉大学中南医院呼吸与危重症学科 湖北 武汉 430071
彭梅婷,女,1997—,医学硕士生,主要从事肺纤维化发病机制相关研究,E‑mail:ppmttt@163.com
刘媛,女,1991—,医学博士,主要从事肺纤维化发病机制相关研究,E‑mail:liuyuanshi33@whu.edu.cn
程真顺,男,1970—,医学博士,教授,主要从事肺纤维化发病机制及急性肺损伤相关研究,E‑mail:zhenshun_cheng@126.com
收稿:2024-12-17,
纸质出版:2025-11-25
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彭梅婷,杨帆,余露等.PPIC敲减通过促进肺成纤维细胞凋亡缓解肺纤维化[J].武汉大学学报(医学版),2025,46(11):1394-1398.
PENG Meiting,YANG Fan,YU Lu,et al.PPIC knockdown promotes lung fibroblasts apoptosis relieve pulmonary fibrosis[J].Medical Journal of Wuhan University,2025,46(11):1394-1398.
彭梅婷,杨帆,余露等.PPIC敲减通过促进肺成纤维细胞凋亡缓解肺纤维化[J].武汉大学学报(医学版),2025,46(11):1394-1398. DOI: 10.14188/j.1671-8852.2024.0983.
PENG Meiting,YANG Fan,YU Lu,et al.PPIC knockdown promotes lung fibroblasts apoptosis relieve pulmonary fibrosis[J].Medical Journal of Wuhan University,2025,46(11):1394-1398. DOI: 10.14188/j.1671-8852.2024.0983.
目的
2
观察肽酰脯氨基顺反异构酶C(PPIC)对肺纤维化小鼠模型及肺成纤维细胞凋亡、活化和细胞外基质(ECM)生成的影响。
方法
2
在不同时期的博来霉素(BLM)肺纤维化小鼠模型中检测PPIC的表达水平,并通过免疫荧光进一步检测PPIC的细胞定位。构建PPIC敲减慢病毒,在BLM肺纤维化小鼠模型中降低PPIC的表达,通过免疫荧光检测肺成纤维细胞的凋亡相关蛋白表达,以及肺组织中胶原的含量。
结果
2
BLM小鼠肺纤维化模型中PPIC含量增加,免疫荧光共染证实PPIC主要表达于肺成纤维细胞中。BLM肺纤维小鼠肺成纤维细胞凋亡较生理盐水组下降,而PPIC的敲减能够有效增加BLM肺纤维化小鼠成纤维细胞的凋亡数量,从而降低肺组织中胶原沉积和成纤维细胞的分化。
结论
2
PPIC敲减促进肺成纤维细胞凋亡、抑制肺成纤维细胞活化及胶原产生从而改善小鼠肺纤维化。
Objective
2
To investigate the effect of peptidyl‑prolyl cis‑trans isomerases C (PPIC) knockdown on pulmonary fibrosis of mice
fibroblast apoptosis
activation
and extracellular matrix (ECM) production.
Methods
2
The expression level of PPIC was detected in Bleomycin(BLM) mouse models of pulmonary fibrosis at different times
and the cellular localization of PPIC was detected by immunofluorescence. PPIC knockdown was constructed with short hairpin RNA (shRNA)
which can reduce the expression of PPIC in a mouse model of BLM⁃induced pulmonary fibrosis. Subsequently
lung fibroblast apoptosis and collagen expression in lung tissues were detected.
Results
2
PPIC expression was increased in bleomycin (BLM)-induced mouse pulmonary fibrosis. Immunofluorescence co-staining showed that PPIC was mainly localized to lung fibroblasts. The number of apoptotic lung fibroblasts in BLM mice was lower than in the saline group
and PPIC knockdown significantly increased the number of apoptotic fibroblasts. More importantly
PPIC knockdown reduced collagen deposition and fibroblast differentiation in the lung tissue of BLM mice.
Conclusion
2
PPIC knockdown inhibits the activation of lung fibroblasts and the production of ECM proteins
thereby ameliorating lung fibrosis in mice.
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