Influence of miR-142-3p on Pulmonary Fibrosis Through Regulation of p53/NF-κB
Ye Shen1, Heng-Jie Li2, Ke Zhang2, Sheng-Qin Li2, Ying-Ge Xu2★★ Corresponding author
- 1Center for Rehabilitation MedicineCenter for Rehabilitation Medicine, Rehabilitation & Sports Medicine Research Institute of Zhejiang Province, Department of Rehabilitation Medicine, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China.
- 2Emergency and Critical Care Center, Department of Emergency Medicine, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, China.
CORRESPONDENCE
Ying-Ge Xu
Emergency and Critical Care Center, Department of Emergency Medicine, Zhejiang Provincial People’s Hospital, Affiliated People’s Hospital, Hangzhou Medical College, Hangzhou, Zhejiang China.
Received: 28-02-2023; Accepted: 25-04-2023.
Volume 14, Issue 1 · pp. 62–71 · PUBLISHED 2023 · DOI: 10.1177/0976500X231175222
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ABSTRACT
Objectives: To investigate the role of miR-142-3p in the bleomycin-induced idiopathic pulmonary fibrosis (IPF) mouse model and elucidate its targets. Methods: In vitro model: Alveolar epithelial cells (AECs) were isolated and treated with bleomycin (50 μg/mL) or PBS for 12 h. In vivo model: Bleomycin (5 mg/kg) was injected into the trachea under anesthesia and aseptic conditions, and controls were treated with equal saline. After the completion of modeling, proteins and RNA were extracted. p53/NF-κB signaling factors were evaluated by western blot or immunohistochemistry. IL-1β and MMP-9 levels were measured by ELISA. The lentiviral transfection technique was used to overexpress miR-142-3p. Results: In IPF, miR-142-3p was identified to play a negative regulatory role in lung epithelial cell senescence. Bleomycin treatment significantly reduced miR-142-3p expression in a concentration-dependent manner in vitro. miR-142-3p overexpression inhibited bleomycin-induced cellular senescence in vivo. In particular, miR-142-3p negatively regulated collagen deposition in pulmonary fibrosis by regulating p53/NF-κB expression. Conclusion: MiR-142-3p plays an important role in the development of IPF by negatively regulating the p53/NF-κB network.
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Shen, Y., Li, H., Zhang, K., Li, S., & Xu, Y. (2023). Influence of miR-142-3p on Pulmonary Fibrosis Through Regulation of p53/NF-κB. Journal of Pharmacology and Pharmacotherapeutics, 14(1), 62–71. https://doi.org/10.1177/0976500X231175222