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MiRNA-21 promotes fibrosis in orbital fibroblasts from thyroid-associated ophthalmopathy #MMPMID25873777
Bo-ding T; Man-Yi X; Jie-Xi Z; Wei X
Mol Vis 2015[]; 21 (ä): 324-34 PMID25873777show ga
Purpose: This study aimed to determine the role of miR-21 in orbital fibroblasts obtained from donors with thyroid-associated ophthalmopathy (TAO) and to elucidate the regulation of fibrosis by miR-21 in the pathological process of TAO. Methods: The expression of miR-21 was investigated in orbital tissues from 26 donors with TAO and 10 donors without TAO. Human orbital fibroblasts were cultivated from TAO donors, and the role of miR-21 in orbital fibroblast proliferation, apoptosis, and differentiation was analyzed. Moreover, the effect of transforming growth factor-beta1 (TGF-?1) on miR-21 expression was also analyzed. In addition, the regulation of miR-21 in TGF-?1-induced collagen production was determined. Results: The expression of miR-21 in orbital fibroblasts from TAO was higher than in donors without TAO. Additional experiments demonstrated that miR-21 enhanced proliferation, decreased apoptosis, and promoted differentiation in TAO orbital fibroblasts. Moreover, this study also showed that TGF-?1 induced miR-21 expression in a time- and dose-dependent manner and miR-21 promoted collagen I mRNA expression and total collagen production induced by TGF-?1. Additionally, miR-21 activated the TGF-?1/Smad signaling pathway by enhancing Smad3 phosphorylation. Conclusions: The present study shows that miR-21 regulates cell proliferation, apoptosis, and differentiation in orbital fibroblasts from TAO, and acts as a mediator in TGF-?1-induced collagen production. These data predict a close association between miR-21 and orbital muscle fibrosis, and provide a novel therapeutic target for TAO.