PURPOSE TGFβ1 is very important in the synthesis and degradation of extracellular matrix (ECM), and also in the mediation of human orbital fibroblasts proliferation. MiR-29 plays an important role in this process in some kinds of fibroblasts. In the present study, the effects of transforming growth factor TGFβ1 on the expression of miR-29 and whether miR-29 is involved in pro-survival signaling pathways mediated by TGFβ1 or not were examined in human orbital fibroblasts(OFs).
METHODS AND RESULTS Treatment of the human OFs with TGFβ1 caused an increase in expression of miR-29a/b/c by real-time PCR analysis. TGFβ1 stimulation increased cell proliferation, colony formation and upregulated expression of COL1A1. Transfecting with miR-29a/b/c mimics reversed TGFβ1-induced phenotype changes in OFs. Western blot analyses showed that TGFβ1 treatment kept total protein expression levels of β-catenin unchanged, but phosphorylation of β-catenin and the expression levels of wnt3a and COL1A1 increased. And miR-29a/b/c mimics interfering blocked DKK1, wnt3a, and phosphorylation of β-catenin and decreased expression of COL1A1 after TGFβ1 treatment.
CONCLUSIONS TGFβ1 activated the wnt/β-catenin pathway, and this activation was essential for the expression of miR-29 inOFs. The results indicate a novel biological function of the wnt/β-catenin pathway in OFs. Elevated expression of miR-29 may play an important role in the pathogenesis of diseases related to fibrogenic reactions in human OFs. |
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