ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Laminin drives survival signals to promote a contractile smooth muscle phenotype and airway hyperreactivity.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Bronchial Thermoplasty Induced Changes in Blood Transcriptome Profile of Patients with Severe Asthma.International journal of molecular sciences · 2026Article
- The Role of Aryl Hydrocarbon Receptor in Airway Remodeling: Mechanistic Insights Across Cellular Functions.Clinical reviews in allergy & immunology · 2026Review
- Analyzing soluble and lung smooth muscle laminin isoform expression in guinea pigs exhibiting various allergic response phenotypes.Frontiers in immunology · 2026Article
- Basement membranes in lung development, disease, and repair.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Impact of CD151 overexpression on prognosis and therapy in non-small cell lung cancer patients lacking EGFR mutations.Cell proliferation · 2024Article
- Transgenic overexpression of α7 integrin in smooth muscle attenuates allergen-induced airway inflammation in a murine model of asthma.FASEB bioAdvances · 2022Article
- Plk1 in Asthma: Ready for Primetime?American journal of respiratory cell and molecular biology · 2022Article
- Pathobiology of Airway Remodeling in Asthma: The Emerging Role of Integrins.Journal of asthma and allergy · 2022Review
- Basement membranes in obstructive pulmonary diseases.Matrix biology plus · 2021Review
- Disruption of AKAP-PKA Interaction Induces Hypercontractility With Concomitant Increase in Proliferation Markers in Human Airway Smooth Muscle.Frontiers in cell and developmental biology · 2020Article
- Integrin α7 expression is increased in asthmatic patients and its inhibition reduces Kras protein abundance in airway smooth muscle cells.Scientific reports · 2019Article
- The cellular origin of laminin determines its role in blood pressure regulation.Cellular and molecular life sciences : CMLS · 2015Article
- Integrins as Therapeutic Targets for Respiratory Diseases.Current molecular medicine · 2015Review
- Airway smooth muscle in airway reactivity and remodeling: what have we learned?American journal of physiology. Lung cellular and molecular physiology · 2013Review
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
Abstract
Increased airway smooth muscle (ASM) mass is believed to underlie the relatively fixed airway hyperresponsiveness (AHR) in asthma. Developments of therapeutic approaches to reverse airway remodeling are impeded by our lack of insight on the mechanisms behind the increase in mass of contractile ASM cells. Increased expression of laminin, an extracellular matrix protein, is associated with asthma. Our studies investigate the role of laminin-induced ASM survival signals in the development of increased ASM and AHR. Antagonizing laminin integrin binding using the laminin-selective competing peptide, YIGSR, and mimicking laminin with exogenous α2-chain laminin, we show that laminin is both necessary and sufficient to induce ASM cell survival, concomitant with the induction of ASM contractile phenotype. Using siRNA, we show that the laminin-binding integrin α7β1 mediates this process. Moreover, in laminin-211-deficient mice, allergen-induced AHR was not observed. Notably, ASM cells from asthmatic airways express a higher abundance of intracellular cell survival proteins, consistent with a role for reduced rates of cell apoptosis in development of ASM hyperplasia. Targeting the laminin-integrin α7β1 signaling pathway may offer new avenues for the development of therapies to reduce the increase in mass of contractile phenotype ASM cells that underlie AHR in asthma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.