Pang Sisi, Chen Bo, Li Yan, Wu Shuangshuang, Chen Lei
Division of Geriatric Cardiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 People's Republic of China.
Division of Geriatric Respiratory, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 People's Republic of China.
Cytotechnology. 2024 Jun;76(3):291-300. doi: 10.1007/s10616-024-00617-2. Epub 2024 Feb 15.
Pulmonary fibrosis (PF) is a chronic lung disease that has a poor prognosis and a serious impact on the quality of life of patients. Here, we investigated the potential role of miR-92a-3p in PF. The mRNA level of miR-92a-3p was significantly increased in both the lung tissues of bleomycin (BLM)--treated mice and pulmonary microvascular endothelial cells (PMVECs). Overexpressing miR-92a-3p increased the mRNA and protein levels of α‑SMA, vimentin, and Col-1 but downregulated E-cadherin. Additionally, the protein and mRNA expression levels of KLF2 were significantly decreased in the lung tissues of BLM-treated mice, suggesting that KLF2 participated in the progression of BLM-induced PF. Downregulating miR-92a-3p upregulated the expression of KLF2 and inhibited the endothelial-to-mesenchymal transition (EndoMT) process, thus alleviating PF in vivo. Altogether, a miR-92a-3p deficiency could significantly reduce the development of myofibroblasts and ameliorate PF progression.
肺纤维化（PF）是一种慢性肺部疾病，预后较差，对患者的生活质量有严重影响。在此，我们研究了miR-92a-3p在PF中的潜在作用。在博来霉素（BLM）处理的小鼠肺组织和肺微血管内皮细胞（PMVECs）中，miR-92a-3p的mRNA水平均显著升高。过表达miR-92a-3p可增加α-SMA、波形蛋白和Col-1的mRNA和蛋白水平，但下调E-钙黏蛋白。此外，BLM处理的小鼠肺组织中KLF2的蛋白和mRNA表达水平显著降低，提示KLF2参与了BLM诱导的PF进展。下调miR-92a-3p可上调KLF2的表达并抑制内皮-间质转化（EndoMT）过程，从而在体内减轻PF。总之，miR-92a-3p缺乏可显著减少肌成纤维细胞的发育并改善PF进展。
