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1 Molecular Pharmacology, University of Groningen, Groningen, Netherlands
* To whom correspondence should be addressed. E-mail: b.g.j.dekkers{at}rug.nl.
Increased airway smooth muscle mass and changes in the ECM are major contributors to airway remodeling. It has recently been demonstrated that ECM proteins may differentially affect proliferation and expression of phenotypic markers of cultured airway smooth muscle (ASM) cells. In the present study, we investigated the functional relevance of ECM proteins in the modulation of ASM contractility using bovine tracheal smooth muscle (BTSM) preparations. The results demonstrate that culturing of BSTM strips for 4 days in the presence of fibronectin or collagen I depressed maximal contraction (Emax) both for methacholine and KCl, which was associated with decreased contractile protein expression. By contrast, both collagen I and fibronectin increased proliferation of cultured BTSM cells. Similar effects were observed for PDGF. Moreover, PDGF augmented fibronectin- and collagen I- induced proliferation in an additive fashion, without an additional effect on contractility or contractile protein expression. The fibronectin-induced depression of contractility was blocked by the integrin antagonist Arg-Gly-Asp-Ser (RGDS) but not by its negative control Gly-Arg-Ala-Asp-Ser-Pro (GRADSP). Laminin, by itself, did not affect contractility or proliferation, but reduced the effects of PDGF on these parameters. Strong relationships were found between the ECM-induced changes in Emax in BTSM strips and their proliferative responses in BSTM cells, and for Emax and contractile protein expression. Our results indicate that ECM proteins differentially regulate both phenotype and function of intact ASM
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