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1-induced connective tissue growth factor (CTGF) expression in airway smooth muscle cells
1 National Heart and Lung Institute, Imperial College, Thoracic Medicine, London, United Kingdom
2 Royal Brompton Hospital, Pathology Department, London, United Kingdom
* To whom correspondence should be addressed. E-mail: f.chung{at}imperial.ac.uk.
Transforming growth factor (TGF)-
may play an important role in airway remodelling and the fibrogenic effect of TGF- mediated through connective tissue growth factor (CTGF) release. We investigated the role of MAPKs and phosphatidylinositol 3-kinase (PI3-K), and the effects of inflammatory cytokines on TGF--induced CTGF expression in human airway smooth muscle cells (ASMC). We examined whether Smad signal was involved in the regulatory mechanisms. TGF-1 induced a time- and concentration-dependent expression of CTGF gene and protein as analysed by real-time RT-PCR and Western blot.
Inhibition of ERK and JNK but not of p38 MAPK and PI3-K blocked the effect of TGF-1 on CTGF mRNA and protein expression and on Smad 2/3 phosphorylation. T helper
lymphocyte 2 (Th2)-derived cytokines, IL-4 and IL-13, attenuated TGF-1-stimulated mRNA and protein expression of CTGF, and inhibited TGF-1-stimulated ERK1/2 and Smad2/3 activation in ASMC. The pro-inflammatory cytokines, TNF-
and IL-1 reduced TGF-1- stimulated mRNA expression of CTGF, but did not inhibit TGF--induced Smad 2/3 phosphorylation. TGF-1-stimulated CTGF expression is mediated by mechanisms involving ERK and JNK pathways, and is down-regulated by IL-4 and IL-13, through modulation of Smad and ERK signals.
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