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2014 ; 5
(5
): e1238
Nephropedia Template TP
gab.com Text
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Integrated analyses identify the involvement of microRNA-26a in
epithelial-mesenchymal transition during idiopathic pulmonary fibrosis
#MMPMID24853416
Liang H
; Gu Y
; Li T
; Zhang Y
; Huangfu L
; Hu M
; Zhao D
; Chen Y
; Liu S
; Dong Y
; Li X
; Lu Y
; Yang B
; Shan H
Cell Death Dis
2014[May]; 5
(5
): e1238
PMID24853416
show ga
Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive, and highly lethal
fibrotic lung disease with poor treatment and unknown etiology. Emerging evidence
suggests that epithelial-mesenchymal transition (EMT) has an important role in
repair and scar formation following epithelial injury during pulmonary fibrosis.
Although some miRNAs have been shown to be dysregulated in the pathophysiological
processes of IPF, limited studies have payed attention on the participation of
miRNAs in EMT in lung fibrosis. In our study, we identified and constructed a
regulation network of differentially expressed IPF miRNAs and EMT genes.
Additionally, we found the downregulation of miR-26a in mice with experimental
pulmonary fibrosis. Further studies showed that miR-26a regulated HMGA2, which is
a key factor in the process of EMT and had the maximum number of regulating
miRNAs in the regulation network. More importantly, inhibition of miR-26a
resulted in lung epithelial cells transforming into myofibroblasts in vitro and
in vivo, whereas forced expression of miR-26a alleviated TGF-?1- and BLM-induced
EMT in A549 cells and in mice, respectively. Taken together, our study deciphered
the essential role of miR-26a in the pathogenesis of EMT in pulmonary fibrosis,
and suggests that miR-26a may be a potential therapeutic target for IPF.