Open AccessMi RNA ‐30a inhibits AEC s‐II apoptosis by blocking mitochondrial fission dependent on Drp‐1
Author(s) -
Mao Cuiping,
Zhang Jinjin,
Lin Shengcui,
Jing Lili,
Xiang Jing,
Wang Meirong,
Wang Bingsi,
Xu Pan,
Liu Weili,
Song Xiaodong,
Lv Changjun
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12420
Subject(s) - mitochondrial fission , apoptosis , transfection , mitochondrion , microbiology and biotechnology , microrna , biology , chemistry , gene , biochemistry
Apoptosis of type II alveolar epithelial cells ( AEC s‐II) is a key determinant of initiation and progression of lung fibrosis. However, the mechanism of miR‐30a participation in the regulation of AEC s‐II apoptosis is ambiguous. In this study, we investigated whether miR‐30a could block AEC s‐II apoptosis by repressing mitochondrial fission dependent on dynamin‐related protein‐1 (Drp‐1). The levels of miR‐30a in vivo and in vitro were determined through quantitative real‐time PCR ( qRT ‐ PCR ). The inhibition of miR‐30a in AEC s‐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 si RNA 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 AEC s‐II apoptosis, inhibit mitochondrial fission, and reduce Drp‐1 expression and translocation. MiR‐30a mimic/inhibitor and Drp‐1 si RNA co‐transfection showed that miR‐30a could inhibit the mitochondrial fission dependent on Drp‐1. This study demonstrated that miR‐30a inhibited AEC s‐II apoptosis by repressing the mitochondrial fission dependent on Drp‐1, and could function as a novel therapeutic target for lung fibrosis.