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.
Keyphrases
- pulmonary fibrosis
- poor prognosis
- endothelial cells
- long non coding rna
- high glucose
- binding protein
- transcription factor
- newly diagnosed
- end stage renal disease
- bone marrow
- stem cells
- gene expression
- chronic kidney disease
- high fat diet induced
- protein protein
- pulmonary hypertension
- peritoneal dialysis
- diabetic rats
- risk assessment
- vascular endothelial growth factor
- mass spectrometry
- small molecule
- adipose tissue
- replacement therapy