Open AccessmicroRNA ‐145‐5p attenuates acute lung injury via targeting ETS2
Author(s) -
Qiao Liang,
Li RongXia,
Hu ShanGang,
Liu Yu,
Liu HongQiang,
Wu HongJun
Publication year - 2022
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12556
Subject(s) - smad , medicine , transforming growth factor , smad2 protein , apoptosis , microrna , lipopolysaccharide , lung , oncogene , cancer research , immunology , endocrinology , cell cycle , biology , cancer , biochemistry , gene
The protective effect of microRNA (miR)‐145‐5p in acute lung injury (ALI) has been discovered previously. Thus, in this study, we attempted to further investigate the mechanism of miR‐145‐5p in ALI through the downstream E26 transformation‐specific proto‐oncogene 2 (ETS2)/transforming growth factor β1 (TGF‐β1)/Smad pathway. A lipopolysaccharide (LPS)‐induced ALI rat model was established. The expression of miR‐145‐5p in ALI rat lung tissues was up‐regulated. Afterward, pathological damage in the lung tissue, the wet/dry (W/D) ratio, apoptosis, and serum inflammatory factor contents were observed. miR‐145‐5p, ETS2, TGF‐β1, Smad2/3, and phosphorylated Smad2/3 levels were measured in rats. miR‐145‐5p expression was down‐regulated, ETS2 expression was up‐regulated, and the TGF‐β1/Smad pathway was activated in LPS‐exposed rats. Overexpression of miR‐145‐5p inactivated the TGF‐β1/Smad pathway and attenuated ALI, as reflected by relieved pathological damage, a decreased W/D ratio, reduced apoptosis, and suppressed inflammatory response. In contrast, loss of miR‐145‐5p or elevated ETS2 levels worsened ALI and activated the TGF‐β1/Smad pathway. Moreover, elevation of ETS2 diminished miR‐145‐5p‐mediated protection against ALI. Evidently, miR‐145‐5p negatively regulates ETS2 expression and inactivates the TGF‐β1/Smad pathway to ameliorate ALI in rats.