成纤维细胞
波形蛋白
SMAD公司
信号转导
下调和上调
转化生长因子
纤维连接蛋白
癌症研究
MAPK/ERK通路
上皮-间质转换
内分泌学
生物
化学
内科学
细胞生物学
细胞培养
医学
免疫学
细胞外基质
免疫组织化学
基因
生物化学
遗传学
作者
Bingyu Xie,Wei Xiong,Feng Zhang,Nuo Wang,Yong Luo,Yizhi Chen,Jiamin Cao,Zhuo-Kun Chen,Chen Ma,Haiyan Chen
标识
DOI:10.1016/j.mce.2022.111780
摘要
Molecular pathways that contribute to orbital fibroblast activation during thyroid-eye disease (TED) may promote TED progression. Non-coding RNAs, especially miRNAs, play a critical role in the pathogenesis of TED. In the present study, miR-103a-3p was dramatically upregulated and TGFBR3 was downregulated within TED orbital tissue samples and TGF-β-stimulated TED orbital fibroblasts. miR-103a-3p inhibition in TGF-β-stimulated TED orbital fibroblasts partially abolished TGF-β-induced fibrotic alterations, as manifested by the impaired fibroblast cell viability and decreased vimentin and fibronectin levels. miR-103a-3p directly targeted TGFBR3 in TED orbital samples and TGF-β-stimulated TED orbital fibroblasts. In TGF-β-stimulated TED orbital fibroblasts, TGFBR3 overexpression inhibited fibroblast cell viability and decreased vimentin and fibronectin levels. TGFBR3 overexpression partially attenuated the inhibitory effects of miR-103a-3p overexpression on TGFBR3 expression and the promotive effects of miR-103a-3p overexpression on TGF-β-induced fibrotic alterations. Under TGF-β stimulation, miR-103a-3p overexpression significantly promoted, whereas TGFBR3 overexpression inhibited the phosphorylation of Erk1/2, JNK, Smad2, and Smad3. TGFBR3 overexpression also partially abolished the effects of miR-103a-3p overexpression on Erk1/2, JNK, Smad2, and Smad3 phosphorylation. In conclusion, the miR-103a-3p/TGFBR3 axis regulated TGF-β-induced TED orbital fibroblast activation and fibrosis in TED, with the possible involvement of the Erk/JNK and TGF-β/Smad signaling pathways.
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