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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Cell Line, Cell Proliferation, Down-Regulation, Extracellular Matrix, Fibroblasts, Humans, MicroRNAs, Orbit, Transforming Growth Factor beta1, Wnt Signaling Pathway.
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Does microRNA-29 mediate TGFβ1-induced extracellular matrix synthesis by targeting wnt/β-catenin pathway in human orbital fibroblasts? Context: Transforming growth factor β1 (TGFβ1) is very important in the synthesis and degradation of extracellular matrix (ECM) and also in the mediation of human orbital fibroblasts (OFs) proliferation. MicroRNA-29 (MiR-29) plays an important role in this process. In the present study, the effects of TGFβ1 on the expression of miR-29 and whether miR-29 is involved in pro-survival signaling pathways mediated by TGFβ1 were examined in human OFs. Detecting the influence of TGFβ1 on the expression of miR-29a/b/c by real-time PCR analysis. Using 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) to detecting the influence of miR-29 on the increased proliferation caused by TGF-β1 on the human orbital fibroblasts. Using soft agar assay to detecting the influence of miR-29 on the increased colony formation caused by TGF-β1 on the human orbital fibroblasts. Western blot was used to detect the specific mechanisin. TGFβ1 treatment decreases the expression of miR-29 in OFs. In the cultured OFs, the value of optical density (OD) in the group treated with miR-29 is lower than that in the group treated without miR-29 (P < 0.05). In the cultured OFs, the ratio of colony formation in the group treated with miR-29 is lower than that in the group treated without miR-29 (P < 0.05). In OFs, miR-29 decreases the secretion of Wnt3a and activation of β-catenin whether the treatment of TGFβ1 was used or not. MiR-29 decreases expression of Collagen, type I, alpha 1 (COL1A1) through down-regulation of wnt/β-catenin pathway.
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In OFs TGFβ1 treatment decreases expression of miR-29 which can cause the inhibition of normal ability of TGFβ1. MiR-29 inhibits TGFβ1-induced proliferation of OFS cell and decreases colony formation of OFS cell after TGFβ1 treatment. MiR-29 Mediates TGFβ1-induced Extracellular matrix synthesis through activation of Wnt/β-catenin pathway in human OFs. Final Decision: yes