NDLI: Smad7 blocks transforming growth factor-ß1-induced gingival fibroblast-myofibroblast transition via inhibitory regulation of Smad2 and connective tissue growth factor.

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Smad7 blocks transforming growth factor-ß1-induced gingival fibroblast-myofibroblast transition via inhibitory regulation of Smad2 and connective tissue growth factor.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sobral, Lays M. Montan, Patrick Franz Zecchin, Karina Gottardello Martelli-Junior, Hercílio Vargas, Pablo Agustin Graner, Edgard Coletta, Ricardo D.
Description	Country affiliation: Brazil Author Affiliation: Sobral LM ( Department of Oral Diagnosis, School of Dentistry, State University of Campinas, Piracicaba, São Paulo, Brazil.)
Abstract	BACKGROUND: Transforming growth factor-ß1 (TGF-ß1), its downstream signaling mediators (Smad proteins), and specific targets, including connective tissue growth factor (CTGF), play important roles in tissue remodeling and fibrosis via myofibroblast activation. We investigated the effect of overexpression of Smad7, a TGF-ß1 signaling inhibitor, on transition of gingival fibroblast to myofibroblast. Moreover, we analyzed the participation of CTGF on TGF-ß1-mediated myofibroblast transformation. METHODS: To study the inhibitory effect of Smad7 on TGF-ß1/CTGF-mediating gingival fibroblast transition into myofibroblasts, we stably overexpressed Smad7 in normal gingival fibroblasts and in myofibroblasts from hereditary gingival fibromatosis (HGF). Myofibroblasts were characterized by the expression of the specific marker isoform of the smooth muscle actin ( -SMA) by Western blot, flow cytometry, and immunofluorescence. Enzyme-linked immunosorbent assay for type I collagen was performed to measure myofibroblast activity. CTGF's role on myofibroblast transformation was examined by enzyme-linked immunosorbent assay and small interference RNA. RESULTS: TGF-ß1 induced the expression of -SMA and CTGF, and small interference RNA-mediating CTGF silencing prevented fibroblast-myofibroblast switch induced by TGF-ß1. In Smad7-overexpressing fibroblasts, ablation of TGF-ß1-induced Smad2 phosphorylation marked decreased -SMA, CTGF, and type I collagen expression. Similarly, HGF transfectants overexpressing Smad7 demonstrated low levels of -SMA and phospho-Smad2 and significant reduction on CTGF and type I collagen production. CONCLUSIONS: CTGF is critical for TGF-ß1-induced gingival fibroblast-myofibroblast transition, and Smad7 overexpression is effective in the blockage of myofibroblast transformation and activation, suggesting that treatments targeting myofibroblasts by Smad7 overexpression may be clinically effective in gingival fibrotic diseases, such as HGF.
File Format	HTM / HTML
ISSN	00223492
Issue Number	4
Volume Number	82
e-ISSN	19433670
Journal	Journal of Periodontology
Language	English
Publisher	American Academy of Periodontology
Publisher Date	2011-04-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Dentistry Cell Transdifferentiation Physiology Fibroblasts Cytology Myofibroblasts Smad7 Protein Transforming Growth Factor Beta1 Metabolism Connective Tissue Growth Factor Gene Expression Regulation Gingiva Humans Signal Transduction Smad2 Protein Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Periodontics

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Cyclosporin A-induced gingival overgrowth is not associated with myofibroblast transdifferentiation

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