Study on plasmacytoma variant translocation gene 1 via transforming growth factor-β1/SMAD pathway promoting excessive fibrosis of endometrial stromal cells
Objective To explore the pathophysiological role and molecular mechanism of long non-coding RNA(lncRNA)plasmacytoma variant translocation gene 1(PVT1)in regulating endometrial stromal cells fibrosis.Methods The expression levels of PVT1,collagen Ⅰ,collagen Ⅲ,transforming growth factor-β1(TGF-β1),SMAD2 and SMAD3 in human endometrial stromal cells(HESCs)were detected by real-time fluorescence quantitative polymerase chain reaction(qRT-PCR).Results Overexpression of PVT1 promoted proliferation of HESCs(P＜0.05),while PVT1 silencing inhibited proliferation of HESCs(P＜0.05).Overexpression of PVT1 up-regulated mRNA expression of collagen Ⅰ and collagen Ⅲ in HESCs(P＜0.05),whereas the mRNA expression levels of collagen Ⅰ and collagen Ⅲ were significantly down-regulated when PVT1 was knocked down(P＜0.05).Overexpression of PVT1 in HESCs could further upregulate the expression of TGF-β1/SMAD signal-related genes(TGF-β1,SMAD2,SMAD3)(P＜0.05).When PVT1 was knocked down,the expression levels of mRNA of TGF-β1/SMAD signal-related genes collagen Ⅰ and collagenⅢ were significantly down-regulated(P＜0.05).PVT1 could induce the production of TGF-β1 in the supernatant of HESCs(P＜0.05).Conclusions PVT1 may promote excessive fibrosis of endometrial stromal cells and produce collagen through the TGF-β1/SMAD pathway.Meanwhile,PVT1 may be a novel target for the treatment of endometrial adhesions.
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维普
