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2017 ; 37
(4
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
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English Wikipedia
The mechanism of TGF-?/miR-155/c-Ski regulates endothelial-mesenchymal transition
in human coronary artery endothelial cells
#MMPMID28607031
Wang J
; He W
; Xu X
; Guo L
; Zhang Y
; Han S
; Shen D
Biosci Rep
2017[Aug]; 37
(4
): ä PMID28607031
show ga
Human coronary artery endothelial cells (HCAECs) have the potential to undergo
fibrogenic endothelial-mesenchymal transition (EndMT), which results in
matrix-producing fibroblasts and thereby contributes to the pathogenesis of
cardiac fibrosis. Recently, the profibrotic cytokine transforming growth factor-?
(TGF-?) is shown to be the crucial pathogenic driver which has been verified to
induce EndMT. C-Ski is an important regulator of TGF-? signaling. However, the
detailed role of c-Ski and the molecular mechanisms by which c-Ski affects
TGF-?-induced EndMT in HCAECs are not largely elucidated. In the present study,
we treated HCAECs with TGF-? of different concentrations to induce EndMT. We
found that overexpression of c-Ski in HCAECs either blocked EndMT via hindering
Vimentin, Snail, Slug, and Twist expression while enhancing CD31 expression, with
or without TGF-? treatment. In contrast, suppression of c-Ski further enhanced
EndMT. Currently, miRNA expression disorder has been frequently reported
associating with cardiac fibrosis. By using online tools, we regarded miR-155 as
a candidate miRNA that could target c-Ski, which was verified using luciferase
assays. C-Ski expression was negatively regulated by miR-155. TGF-?-induced EndMT
was inhibited by miR-155 silence; the effect of TGF-? on Vimentin, CD31, Snail,
Slug, and Twist could be partially restored by miR-155. Altogether, these
findings will shed light on the role and mechanism by which miR-155 regulates
TGF-?-induced HCAECs EndMT via c-Ski to affect cardiac fibrosis, and
miR-155/c-Ski may represent novel biomarkers and therapeutic targets in the
treatment of cardiac fibrosis.
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