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1-induced connective tissue growth factor expression in airway smooth muscle cells
1Thoracic Medicine, National Heart and Lung Institute, Imperial College and 2Pathology Department, Royal Brompton Hospital, London, United Kingdom
Submitted 30 April 2004 ; accepted in final form 12 September 2004
Transforming growth factor (TGF)-
may play an important role in airway remodeling, and the fibrogenic effect of TGF- may be mediated through connective tissue growth factor (CTGF) release. We investigated the role of MAPKs and phosphatidylinositol 3-kinase (PI3K) 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 analyzed by real-time RT-PCR and Western blot. Inhibition of ERK and c-jun NH2-terminal kinase (JNK), but not of p38 MAPK and PI3K, blocked the effect of TGF-1 on CTGF mRNA and protein expression and on Smad2/3 phosphorylation. T helper lymphocyte 2-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 proinflammatory cytokines tumor necrosis factor-
and IL-1 reduced TGF-1-stimulated mRNA expression of CTGF but did not inhibit TGF--induced Smad2/3 phosphorylation. TGF-1-stimulated CTGF expression is mediated by mechanisms involving ERK and JNK pathways and is downregulated by IL-4 and IL-13 through modulation of Smad and ERK signals.
mitogen-activated protein kinases; signal transduction; Smad; cytokines; asthma; transforming growth factor
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