5-Fluorouracil Blocks Transforming Growth Factor-β–Induced α2 Type I Collagen Gene (COL1A2) Expression in Human Fibroblasts via c-Jun NH2-Terminal Kinase/Activator Protein-1 Activation

2003 ◽  
Vol 64 (3) ◽  
pp. 707-713 ◽  
Author(s):  
Jeanne Wendling ◽  
Aimé Marchand ◽  
Alain Mauviel ◽  
Franck Verrecchia
Keyword(s):  
Growth Factor ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Human Fibroblasts ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Collagen Gene ◽  
Activator Protein 1 ◽  
Activator Protein

A nuclear factor 1 binding site mediates the transcriptional activation of a type I collagen promoter by transforming growth factor-β

Cell ◽  
1988 ◽  
Vol 52 (3) ◽  
pp. 405-414 ◽  
Author(s):  
Pellegrino Rossi ◽  
Gerard Karsenty ◽  
Anita B. Roberts ◽  
Nanette S. Roche ◽  
Michael B. Sporn ◽  
...  
Keyword(s):  
Growth Factor ◽  
Binding Site ◽  
Transcriptional Activation ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Nuclear Factor ◽  
Nuclear Factor 1 ◽  
Collagen Promoter

scholarly journals The pentapeptide KTTKS promoting the expressions of type I collagen and transforming growth factor-β of tendon cells

2007 ◽  
Vol 25 (12) ◽  
pp. 1629-1634 ◽  
Author(s):  
Wen-Chung Tsai ◽  
Chih-Chin Hsu ◽  
Chia-Ying Chung ◽  
Miao-Sui Lin ◽  
Sung-Lung Li ◽  
...  
Keyword(s):  
Growth Factor ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Tendon Cells

AP-1 overexpression impairs corticosteroid inhibition of collagen production by fibroblasts isolated from asthmatic subjects

2010 ◽  
Vol 299 (2) ◽  
pp. L281-L287 ◽  
Author(s):  
Eric Jacques ◽  
Abdelhabib Semlali ◽  
Louis Philippe Boulet ◽  
Jamila Chakir
Keyword(s):  
Protein Expression ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Inhaled Corticosteroids ◽  
Airway Remodeling ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Activator Protein 1 ◽  
Western Blots ◽  
Collagen Production

Asthma is characterized by airway remodeling associated with an increase in the deposition of ECM proteins such as type I collagen. These components are mainly produced by fibroblasts. Inhaled corticosteroids are considered the cornerstone of asthma therapy. Despite substantial evidence as to the anti-inflammatory action of corticosteroids, their effect on controlling ECM protein deposition in the airways is not completely understood. This study determined the effect of dexamethasone (Dex) on collagen production by bronchial fibroblasts derived from asthmatic and healthy subjects. Expression of procollagen mRNA in fibroblasts from asthmatics and normal controls was determined by quantitative PCR. Regulation of the procollagen-α1I promoter was evaluated by transient transfections. Transforming growth factor-β (TGF-β) protein expression was determined by ELISA. Protein expression of glucocorticoid receptor (GR) and interaction with activator protein-1 (AP-1), a collagen regulatory transcription factor, was assessed by Western blots, coimmunoprecipitations, and EMSA. AP-1 overexpression was performed by transient transfection using c-Fos/c-Jun expression plasmids. Dex significantly downregulated procollagen production and promoter activity in normal fibroblasts but had no effect on asthmatic fibroblasts. AP-1 and GR interaction increased after Dex stimulation in asthmatic fibroblasts. AP-1 overexpression in control fibroblasts abrogated collagen gene response to Dex. These results show that Dex failed to reduce collagen production in fibroblasts from asthmatic subjects. This impaired response may be related to AP-1 overexpression in these cells.

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