ArticleNature biomedical engineering2019
A microphysiological model of the bronchial airways reveals the interplay of mechanical and biochemical signals in bronchospasm.
Article in Nature biomedical engineering, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
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- Modeling immunity in microphysiological systems.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Pseudomonas aeruginosa type IV pili actively induce mucus contraction to form biofilms in tissue-engineered human airways.PLoS biology · 2023Article
- Organ-on-a-chip technologies for biomedical research and drug development: A focus on the vasculature.Smart medicine · 2023Article
- Thrombin induces IL-8/CXCL8 expression by DCLK1-dependent RhoA and YAP activation in human lung epithelial cells.Journal of biomedical science · 2022Article
- What Can an Organ-on-a-Chip Teach Us About Human Lung Pathophysiology?Physiology (Bethesda, Md.) · 2022Review
- Inhibition of ABCC1 Decreases cAMP Egress and Promotes Human Airway Smooth Muscle Cell Relaxation.American journal of respiratory cell and molecular biology · 2022Article
- Engineered Tools to Study Intercellular Communication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- The odorant receptor OR2W3 on airway smooth muscle evokes bronchodilation via a cooperative chemosensory tradeoff between TMEM16A and CFTR.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Microphysiological systems for the modeling of wound healing and evaluation of pro-healing therapies.Journal of materials chemistry. B · 2020Review
- Unleashing shear: Role of intercellular traction and cellular moments in collective cell migration.Biochemical and biophysical research communications · 2020Article
- A microphysiological model of the bronchial airways reveals the interplay of mechanical and biochemical signals in bronchospasm.Nature biomedical engineering · 2019Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
In asthma, the contraction of the airway smooth muscle and the subsequent decrease in airflow involve a poorly understood set of mechanical and biochemical events. Organ-level and molecular-scale models of the airway are frequently based on purely mechanical or biochemical considerations and do not account for physiological mechanochemical couplings. Here, we present a microphysiological model of the airway that allows for the quantitative analysis of the interactions between mechanical and biochemical signals triggered by compressive stress on epithelial cells. We show that a mechanical stimulus mimicking a bronchospastic challenge triggers the marked contraction and delayed relaxation of airway smooth muscle, and that this is mediated by the discordant expression of cyclooxygenase genes in epithelial cells and regulated by the mechanosensor and transcriptional co-activator Yes-associated protein. A mathematical model of the intercellular feedback interactions recapitulates aspects of obstructive disease of the airways, which include pathognomonic features of severe difficult-to-treat asthma. The microphysiological model could be used to investigate the mechanisms of asthma pathogenesis and to develop therapeutic strategies that disrupt the positive feedback loop that leads to persistent airway constriction.
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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.