title: MicroRNA-29 mediates TGFβ1-induced extracellular matrix synthesis by targeting wnt/β-catenin pathway in human orbital fibroblasts.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Ophthalmology, The Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Tan
authors.affiliation: Department of Ophthalmology and Eye Research Center, The Second Xiangya Hospital, Central South University Changsha 410011, Hunan, China.
authors.forename: Bo-Ding
authors.initials: BD
authors.lastname: Tong
authors.affiliation: Department of Ophthalmology and Eye Research Center, The Second Xiangya Hospital, Central South University Changsha 410011, Hunan, China.
authors.forename: Yu-Jie
authors.initials: YJ
authors.lastname: Wu
authors.affiliation: Department of Ophthalmology and Eye Research Center, The Second Xiangya Hospital, Central South University Changsha 410011, Hunan, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Xiong
mesh_terms: D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects / Q000502:physiology; D015536:Down-Regulation / Q000187:drug effects; D005109:Extracellular Matrix / Q000187:drug effects / Q000378:metabolism*; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009915:Orbit / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology*; D060449:Wnt Signaling Pathway / Q000187:drug effects / Q000502:physiology*
chemical_list: C532045:MIRN29a microRNA, human; D035683:MicroRNAs; D053773:Transforming Growth Factor beta1
keywords: Orbital fibrosis; TGFβ1; miR-29; wnt/β-catenin pathway