ArticleRespiratory research2010
The laminin β1-competing peptide YIGSR induces a hypercontractile, hypoproliferative airway smooth muscle phenotype in an animal model of allergic asthma.
Article in Respiratory research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- In-Depth Analysis of AG73-Dental Pulp Cell Interactions Underlying Adhesion and Mineralization: Insights from Alanine Scanning.Tissue engineering and regenerative medicine · 2026Article
- Bronchial Thermoplasty Induced Changes in Blood Transcriptome Profile of Patients with Severe Asthma.International journal of molecular sciences · 2026Article
- Analyzing soluble and lung smooth muscle laminin isoform expression in guinea pigs exhibiting various allergic response phenotypes.Frontiers in immunology · 2026Article
- Basement membranes in obstructive pulmonary diseases.Matrix biology plus · 2021Review
- Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021Article
- Important lessons learned from studies on the pharmacology of glucocorticoids in human airway smooth muscle cells: Too much of a good thing may be a problem.Pharmacology & therapeutics · 2020Review
- Integrin α7 expression is increased in asthmatic patients and its inhibition reduces Kras protein abundance in airway smooth muscle cells.Scientific reports · 2019Article
- NeonatalBioMed research international · 2019Article
- Airway remodeling in asthma: what really matters.Cell and tissue research · 2017Review
- Laminin drives survival signals to promote a contractile smooth muscle phenotype and airway hyperreactivity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Integrin β1 regulates leiomyoma cytoskeletal integrity and growth.Matrix biology : journal of the International Society for Matrix BiologyArticle
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFibroproliferative 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.
methodsUsing 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.
resultsTopical 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 antagonized by soluble YIGSR.
conclusionThese results indicate that the laminin-competing peptide YIGSR promotes a contractile, hypoproliferative ASM phenotype in vivo, an effect that appears to be linked to the microenvironment in which the cells are exposed to the peptide.
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