ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Focal adhesion kinase (FAK) and mechanical stimulation negatively regulate the transition of airway smooth muscle tissues to a synthetic phenotype.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Observational
- Membrane adhesion junctions regulate airway smooth muscle phenotype and function.Physiological reviews · 2023Review
- 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
- Molecular mechanisms of voiding dysfunction in a novel mouse model of acute urinary retention.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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
- 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
- Inhibition of protein FAK enhances 5-FU chemosensitivity to gastric carcinomaComputational and structural biotechnology journal · 2020Article
- 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
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The effects of mechanical forces and focal adhesion kinase (FAK) in regulating the inflammatory responses of airway smooth muscle (ASM) tissues to stimulation with interleukin (IL)-13 were investigated. Canine tracheal tissues were subjected to different mechanical loads in vitro, and the effects of mechanical load on eotaxin secretion and inflammatory signaling pathways in response to IL-13 were determined. Eotaxin secretion by tissues in response to IL-13 was significantly inhibited in muscles maintained at a higher (+) load compared with those at a lower (-) load as assessed by ELISA, and Akt activation was also reduced in the higher (+) loaded tissues. Conversely the (+) mechanical load increased activation of the focal adhesion proteins FAK and paxillin in the tissues. The role of FAK in regulating the mechanosensitive responses was assessed by overexpressing FAK-related nonkinase in the tissues, by expressing the FAK kinase-dead mutant FAK Y397F, or by treating tissues with the FAK inhibitor PF-573228. FAK inactivation potentiated Akt activity and increased eotaxin secretion in response to IL-13. FAK inhibition also suppressed the mechanosensitivity of Akt activation and eotaxin secretion. In addition, FAK inactivation suppressed smooth muscle myosin heavy chain expression induced by the higher (+) mechanical load. The results demonstrate that the imposition of a higher mechanical load on airway smooth muscle stimulates FAK activation, which promotes the expression of the differentiated contractile phenotype and suppresses the synthetic phenotype and the inflammatory responses of the muscle tissue.
Indexed as
Identifiers
What OpenQuestion holds
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.