ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Mechanical stimuli and IL-13 interact at integrin adhesion complexes to regulate expression of smooth muscle myosin heavy chain in airway smooth muscle tissue.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Use of continuous positive airway pressure reduces airway reactivity in adults with asthma.The European respiratory journal · 2013Trial
- Interleukin-13 R130Q aggravates airway smooth-muscle phenotypic switching and promotes airway remodeling in severe asthma.Frontiers in physiology · 2026Article
- Nasal microRNA signatures for disease severity in infants with respiratory syncytial virus bronchiolitis: a multicentre prospective study.BMJ open respiratory research · 2024Article
- Membrane adhesion junctions regulate airway smooth muscle phenotype and function.Physiological reviews · 2023Review
- Destructive fibrotic teamwork: how both microenvironment stiffness and profibrotic interleukin 13 impair alveolar macrophage phenotype and function.Biomaterials science · 2022Article
- Noncanonical HIPPO/MST Signaling via BUB3 and FOXO Drives Pulmonary Vascular Cell Growth and Survival.Circulation research · 2022Article
- The proprotein convertase furin inhibits IL-13-induced inflammation in airway smooth muscle by regulating integrin-associated signaling complexes.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- S100A4 is activated by RhoA and catalyses the polymerization of non-muscle myosin, adhesion complex assembly and contraction in airway smooth muscle.The Journal of physiology · 2020Article
- Continuous Positive Airway Pressure (CPAP) in Non-Apneic Asthma: A Clinical Review of Current Evidence.Turkish thoracic journal · 2020Review
- S100A4 is secreted by airway smooth muscle tissues and activates inflammatory signaling pathways via receptors for advanced glycation end products.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Phenotype transitions induced by mechanical stimuli in airway smooth muscle are regulated by differential interactions of parvin isoforms with paxillin and Akt.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Airway smooth muscle adapting in dynamic conditions is refractory to the bronchodilator effect of a deep inspiration.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Apoptosis Induction and Alteration of Cell Adherence in Human Lung Cancer Cells under Simulated Microgravity.International journal of molecular sciences · 2019Article
- Effect of CPAP on airway reactivity and airway inflammation in children with moderate-severe asthma.Respirology (Carlton, Vic.) · 2019Article
- Molecular Mechanisms for the Mechanical Modulation of Airway Responsiveness.Journal of engineering and science in medical diagnostics and therapy · 2019Article
- NeonatalBioMed research international · 2019Article
- Rho kinase collaborates with p21-activated kinase to regulate actin polymerization and contraction in airway smooth muscle.The Journal of physiology · 2018Article
- Elastase alters contractility and promotes an inflammatory synthetic phenotype in airway smooth muscle tissues.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Non-muscle (NM) myosin heavy chain phosphorylation regulates the formation of NM myosin filaments, adhesome assembly and smooth muscle contraction.The Journal of physiology · 2017Article
- Personalised medicine in asthma: from curative to preventive medicine.European respiratory review : an official journal of the European Respiratory Society · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Airway smooth muscle phenotype may be modulated in response to external stimuli under physiological and pathophysiological conditions. The effect of mechanical forces on airway smooth muscle phenotype were evaluated in vitro by suspending weights of 0.5 or 1 g from the ends of canine tracheal smooth muscle tissues, incubating the weighted tissues for 6 h, and then measuring the expression of the phenotypic marker protein, smooth muscle myosin heavy chain (SmMHC). Incubation of the tissues at a high load significantly increased expression of SmMHC compared with incubation at low load. Incubation of the tissues at a high load also decreased activation of PKB/Akt, as indicated by its phosphorylation at Ser 473. Inhibition of Akt or phosphatidylinositol-3,4,5 triphosphate-kinase increased SmMHC expression in tissues at low load but did not affect SmMHC expression at high load. IL-13 induced a significant increase in Akt activation and suppressed the expression of SmMHC protein at both low and high loads. The role of integrin signaling in mechanotransduction was evaluated by expressing a PINCH (LIM1-2) fragment in the muscle tissues that prevents the membrane localization of the integrin-binding IPP complex (ILK/PINCH/α-parvin), and also by expressing an inactive integrin-linked kinase mutant (ILK S343A) that inhibits endogenous ILK activity. Both mutants inhibited Akt activation and increased expression of SmMHC protein at low load but had no effect at high load. These results suggest that mechanical stress and IL-13 both act through an integrin-mediated signaling pathway to oppositely regulate the expression of phenotypic marker proteins in intact airway smooth muscle tissues. The stimulatory effects of mechanical stress on contractile protein expression oppose the suppression of contractile protein expression mediated by IL-13; thus the imposition of mechanical strain may inhibit changes in airway smooth muscle phenotype induced by inflammatory mediators.
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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.