☆ 4.6 Article

The microRNA miR-17 regulates lung FoxA1 expression during lipopolysaccharide-induced acute lung injury

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS (2014)

期刊

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

卷 445, 期 1, 页码 48-53

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE

DOI: 10.1016/j.bbrc.2014.01.108

关键词

Acute lung injury; Alveolar type II epithelial cells; FoxA1; miR-17; Gene expression

类别

Biochemistry & Molecular Biology Biophysics

资金

Nature Science Foundation of China [81000026]
Natural Science Foundation of Hunan Province, China [14JJ7060]
Science and Technology Project of Hunan Province, China [2013SK3077]
Research Foundation of Education Bureau of Hunan Province, China [13C691]
Research Foundation of Stem Cell Regulation and Application, Hunan University of Chinese Medicine, China [2013GXB01]

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摘要

Acute lung injury (ALI) is a severe pulmonary disease that causes a high number of fatalities worldwide. Studies have shown that FoxA1 expression is upregulated during ALI and may play an important role in ALI by promoting the apoptosis of alveolar type II epithelial cells. However, the mechanism of FoxA1 overexpression in ALI is unclear. In this study, an in vivo murine model of ALI and alveolar type II epithelial cells injury was induced using lipopolysaccharide (LPS). LPS upregulated FoxA1 in the lung tissue of the in vivo ALI model and in LPS-challenged type II epithelial cells. In contrast, miR-17 was significantly downregulated in these models. After miR-17 antagomir injection, the expression of FoxA1 was significantly increased in ALI mice. MiR-17 mimics could significantly inhibit FoxA1 mRNA and protein expression, whereas the miR-17 inhibitor could significantly increase FoxA1 mRNA and protein expression in LPS-induced type II epithelial cells. Thus, our results suggest that the downregulation of miR-17 expression could lead to FoxA1 overexpression in ALI. (C) 2014 Elsevier Inc. All rights reserved.

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