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Báo cáo y học: "The laminin b1-competing peptide YIGSR induces a hypercontractile, hypoproliferative airway smooth muscle phenotype in an animal model of allergic asthma"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:The laminin b1-competing peptide YIGSR induces a hypercontractile, hypoproliferative airway smooth muscle phenotype in an animal model of allergic asthma. | Dekkers et al. Respiratory Research 2010 11 170 http respiratory-research.eom content 11 1 170 RESPIRATORY RESEARCH RESEARCH Open Access The laminin b1-competing peptide YIGSR induces a hypercontractile hypoproliferative airway smooth muscle phenotype in an animal model of allergic asthma 1 1 2 1 1 Bart GJ Dekkers I Sophie T Bos Andrew J Halayko Johan Zaagsma Herman Meurs Abstract Background Fibroproliferative airway remodelling including increased airway smooth muscle ASM mass and contractility contributes to airway hyperresponsiveness in asthma. In vitro studies have shown that maturation of ASM cells to a hyper contractile phenotype is dependent on laminin which can be inhibited by the laminin-competing peptide Tyr-Ile-Gly-Ser-Arg YIGSR . The role of laminins in ASM remodelling in chronic asthma in vivo however has not yet been established. Methods Using an established guinea pig model of allergic asthma we investigated the effects of topical treatment of the airways with YIGSR on features of airway remodelling induced by repeated allergen challenge including ASM hyperplasia and hypercontractility inflammation and fibrosis. Human ASM cells were used to investigate the direct effects of YIGSR on ASM proliferation in vitro. Results Topical administration of YIGSR attenuated allergen-induced ASM hyperplasia and pulmonary expression of the proliferative marker proliferating cell nuclear antigen PCNA . Treatment with YIGSR also increased both the expression of sm-MHC and ASM contractility in saline- and allergen-challenged animals this suggests that treatment with the laminin-competing peptide YIGSR mimics rather than inhibits laminin function in vivo. In addition treatment with YIGSR increased allergen-induced fibrosis and submucosal eosinophilia. Immobilized YIGSR concentration-dependently reduced PDGF-induced proliferation of cultured ASM to a similar extent as laminin-coated culture plates. Notably the effects of both immobilized YIGSR and laminin were .