MiRNA‐30a inhibits AECs‐II apoptosis by blocking mitochondrial fission dependent on Drp‐1. Issue 12 (6th October 2014)

• Record Type: Journal Article
• Authors: Mao, Cuiping; Zhang, Jinjin; Lin, Shengcui; Jing, Lili; Xiang, Jing; Wang, Meirong; Wang, Bingsi; Xu, Pan; Liu, Weili; Song, Xiaodong; Lv, Changjun
• Is Part Of: Journal of cellular and molecular medicine. Volume 18:Issue 12(2014)
• Page Start: 2404
• Page End: 2416
• Publication Date: 2014-10-06
• Subjects: Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.12420
• Languages: English
• ISSNs: 1582-1838

Abstract

<abstract abstract-type="main" id="jcmm12420-abs-0001"> <title>Abstract</title> <p>Apoptosis of type II alveolar epithelial cells (AECs‐II) is a key determinant of initiation and progression of lung fibrosis. However, the mechanism of miR‐30a participation in the regulation of AECs‐II apoptosis is ambiguous. In this study, we investigated whether miR‐30a could block AECs‐II apoptosis by repressing mitochondrial fission dependent on dynamin‐related protein‐1 (Drp‐1). The levels of miR‐30a <italic>in vivo</italic> and <italic>in vitro</italic> were determined through quantitative real‐time PCR (qRT‐PCR). The inhibition of miR‐30a in AECs‐II apoptosis, mitochondrial fission and its dependence on Drp‐1, and Drp‐1 expression and translocation were detected using miR‐30a mimic, inhibitor‐transfection method (gain‐ and loss‐of‐function), or Drp‐1 siRNA technology. Results showed that miR‐30a decreased in lung fibrosis. Gain‐ and loss‐of‐function studies revealed that the up‐regulation of miR‐30a could decrease AECs‐II apoptosis, inhibit mitochondrial fission, and reduce Drp‐1 expression and translocation. MiR‐30a mimic/inhibitor and Drp‐1 siRNA co‐transfection showed that miR‐30a could inhibit the mitochondrial fission dependent on Drp‐1. This study demonstrated that miR‐30a inhibited AECs‐II apoptosis by repressing the mitochondrial fission dependent on Drp‐1, and could function as a novel therapeutic target for lung fibrosis.</p> </abstract>