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MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic
Cataracts Through Targeting SNAI1
#MMPMID28442786
Zhang L
; Wang Y
; Li W
; Tsonis PA
; Li Z
; Xie L
; Huang Y
Sci Rep
2017[Apr]; 7
(1
): 1117
PMID28442786
show ga
Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental
process in development, fibrosis, and metastasis. During the process, epithelial
cells lose their morphology and transcriptional program, and transdifferentiate
to mesenchymal cells. It has been reported that lens epithelial cells undergo EMT
during cataract formation, and regulation of microRNAs on genes is associated
with lens development. However, the molecular mechanisms of this regulation in
diabetic cataract still need to be investigated. In the present study, the
expression of E-cadherin was downregulated, while the expression of alpha-SMA and
vimentin was upregulated in diabetic cataract tissues and the in vitro model,
suggesting the involvement of EMT in diabetic cataract formation. Results of
miRNA profiling demonstrated that miR-30a was markedly downregulated in diabetic
cataract tissues. Overexpression of miR-30a-5p decreased SNAI1, a known modulator
of EMT, and the expression of vimentin and alpha-SMA in our diabetic cataract
model in vitro. It is concluded that EMT is involved in human diabetic cataract,
and upregulation of miR-30a can repress EMT through its targeting of SNAI1 in
lens epithelial cells, which make miR-30a a novel target of therapeutic
intervention for human diabetic cataract.
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