NDLI: N-acetyl-L-cysteine inhibits TGF-beta1-induced profibrotic responses in fibroblasts.

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N-acetyl-L-cysteine inhibits TGF-beta1-induced profibrotic responses in fibroblasts.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sugiura, Hisatoshi Ichikawa, Tomohiro Liu, Xiangde Kobayashi, Tetsu Wang, Xing Qi Kawasaki, Shin Togo, Shinsaku Kamio, Koichiro Mao, Lijun Ann, Youngsoo Ichinose, Masakazu Rennard, Stephen I.
Description	Country affiliation: Japan Author Affiliation: Sugiura H ( Third Department of Internal Medicine, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama, Wakayama 641-0012, Japan. sugiura@wakayama-med.ac.jp)
Abstract	BACKGROUND: Excessive production of TGF-beta(1) plays a key role in the tissue remodeling or fibrotic process observed in bronchial asthma, chronic pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). TGF-beta(1) has been reported to decrease the intracellular glutathione level and stimulate the production of reactive oxygen species. OBJECTIVES: The aim of this study was to evaluate whether the antioxidant N-acetyl-l-cysteine (NAC) can affect TGF-beta(1)-mediated tissue remodeling in fibroblasts or modulate the production of fibronectin and vascular endothelial growth factor (VEGF) which are believed to be important mediators of tissue repair and remodeling. METHODS: To accomplish this, human fetal lung fibroblasts (HFL-1) were used to assess the effect of NAC on the TGF-beta(1)-mediated contraction of floating gels and the TGF-beta(1)-induced mediator production. In addition, the effect of NAC on the TGF-beta(1)-induced differentiation to myofibroblasts was evaluated by assessing alpha-smooth muscle actin (alpha-SMA) expression. RESULTS: NAC significantly abolished the TGF-beta(1)-augmented gel contraction (at 3mM, gel size 63.4+/-2.6% vs. 39.1+/-4.1%; p<0.01) compared with control in a concentration-dependent manner. NAC also significantly inhibited the TGF-beta(1)-augmented fibronectin (p<0.01) and VEGF (p<0.01) production in the media of both the three-dimensional gel and monolayer culture. Furthermore, NAC reversed the TGF-beta(1)-stimulated alpha-SMA expression (p<0.01). CONCLUSION: These results suggest that NAC can affect the TGF-beta(1)-induced tissue remodeling or fibrotic process in vitro.
File Format	HTM / HTML
ISSN	10945539
Issue Number	6
Volume Number	22
e-ISSN	15229629
Journal	Pulmonary Pharmacology & Therapeutics
Language	English
Publisher	Elsevier
Publisher Date	2009-12-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Pharmacology Discipline Pulmonary Medicine Acetylcysteine Pharmacology Fibroblasts Drug Effects Pathology Transforming Growth Factor Beta1 Antagonists & Inhibitors Toxicity Actins Biosynthesis Genetics Animals Blotting, Western Cells, Cultured Collagen Type I Enzyme-linked Immunosorbent Assay Fibronectins Fibrosis Humans Rats Vascular Endothelial Growth Factor A Journal Article
Content Type	Text
Resource Type	Article
Subject	Biochemistry (medical) Pulmonary and Respiratory Medicine Pharmacology (medical)

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