TGF mediates collagen production in human CRSsNP nasal mucosa-derived fibroblasts through Smad2/3-dependent pathway and CTGF induction and secretion

doi:10.1002/jcp.27718

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Title:	TGF mediates collagen production in human CRSsNP nasal mucosa-derived fibroblasts through Smad2/3-dependent pathway and CTGF induction and secretion
Authors:	Jiunn-Min Shieh(謝俊民) Tsai, Yih-Jeng Chi, Jessie Chao-Yun Wu, Wen-Bin
Contributors:	Chi Mei Med Ctr, Dept Internal Med Chia Nan Univ Pharm & Sci, Dept Recreat & Healthcare Management Shin Kong Wu Ho Mem Hosp, Dept Otolaryngol Head & Neck Surg Fu Jen Catholic Univ, Sch Med, Coll Med Minist Hlth & Welf, Taichung Hosp, Dept Otolaryngol Head & Neck Surg Chung Shan Med Univ, Inst Med
Keywords:	cellular signaling CRS CTGF extracellular matrix tissue remodeling
Date:	2019-07
Issue Date:	2020-07-29 13:49:08 (UTC+8)
Publisher:	WILEY
Abstract:	Chronic rhinosinusitis without nasal polyp (CRSsNP) is characterized by tissue remodeling and fibrosis. Transforming growth factor- (TGF-) is considered a master switch in the induction of the profibrotic program which can induce fibroblasts to synthesize and contract extracellular matrix (ECM) proteins. A previous study has shown TGF-1 signaling and collagen overproduction in the CRSsNP, but the responsible cells and mechanism of action remain unclear. Therefore, this study was aimed to investigate the relationship between TGF-1 stimulation and collagen expression and to explore the role of connective tissue growth factor (CTGF) during the remodeling process using human CRSsNP nasal mucosa tissues and mucosa-derived fibroblasts as main materials. We found that TGF-1 and its isoforms could promote collagen protein expression. Concomitantly, TGF-1 caused CTGF expression and secretion. An addition of exogenous CTGF to fibroblasts also caused collagen expression. In accordance with these observations, TGF-1, CTGF, and collagen were highly expressed in the subepithelial stroma region of CRSsNP nasal mucosa, as determined by immunohistochemistry. The TGF-1-mediated collagen expression could be blocked by actinomycin D and SIS3, suggesting that the induction was through transcriptional regulation and Smad2/3-dependent pathway. Finally, we demonstrated that CTGF small interfering RNA knockdown led to a substantial decrease in TGF-1-mediated collagen expression. Collectively, our results provide first and further evidence that TGF-1 mediates collagen expression-production through a canonical Smad2/3-dependent pathway and CTGF induction and secretion in human nasal fibroblasts. Moreover, TGF-1, CTGF, and collagen are highly expressed in human CRSsNP nasal mucosa specimens, suggesting their roles in tissue remodeling during CRSsNP progression.
Relation:	Journal of Cellular Physiology, v.234, n.7, pp.10489-10499
Appears in Collections:	[Dept. of Recreation and Health-Care Management] Periodical Articles

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