ArticleBiophysical journal2010
A mathematical analysis of agonist- and KCl-induced Ca(2+) oscillations in mouse airway smooth muscle cells.
Article in Biophysical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Characterization of PDGF-Induced Subcellular Calcium Regulation through Calcium Channels in Airway Smooth Muscle Cells by FRET Biosensors.Biosensors · 2024Article
- Neural regulation of slow waves and phasic contractions in the distal stomach: a mathematical model.Journal of neural engineering · 2024Article
- Inherent differences of small airway contraction and CaFrontiers in cell and developmental biology · 2023Article
- Airway smooth muscle and airway hyperresponsiveness in asthma: mechanisms of airway smooth muscle dysfunction.Minerva medica · 2022Article
- Reciprocal Correlations of Inflammatory and Calcium Signaling in Asthma Pathogenesis.Advances in experimental medicine and biology · 2021Article
- A Model ofBulletin of mathematical biology · 2019Article
- The relative contributions of store-operated and voltage-gated CaThe Journal of physiology · 2017Article
- Inhibition of PI3K promotes dilation of human small airways in a rho kinase-dependent manner.British journal of pharmacology · 2016Article
- Ryanodine receptor sensitization results in abnormal calcium signaling in airway smooth muscle cells.American journal of respiratory cell and molecular biology · 2015Article
- Suppression of the increasing level of acetylcholine-stimulated intracellular CaBiomedical reports · 2015Article
- Phenotype, endotype and patient-specific computational modelling for optimal treatment design in asthma.Drug discovery today. Disease models · 2015Article
- A deterministic model predicts the properties of stochastic calcium oscillations in airway smooth muscle cells.PLoS computational biology · 2014Article
- Computational modeling of anoctamin 1 calcium-activated chloride channels as pacemaker channels in interstitial cells of Cajal.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Activation of store-operated calcium entry in airway smooth muscle cells: insight from a mathematical model.PloS one · 2013Article
- Review
- A multi-scale approach to airway hyperresponsiveness: from molecule to organ.Frontiers in physiology · 2012Article
- Multiscale mathematical models of airway constriction and disease.Pulmonary pharmacology & therapeutics · 2011Review
- Exploring lung physiology in health and disease with lung slices.Pulmonary pharmacology & therapeutics · 2011Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway hyperresponsiveness is a major characteristic of asthma and is generally ascribed to excessive airway narrowing associated with the contraction of airway smooth muscle cells (ASMCs). ASMC contraction is initiated by a rise in intracellular calcium concentration ([Ca(2+)](i)), observed as oscillatory Ca(2+) waves that can be induced by either agonist or high extracellular K(+) (KCl). In this work, we present a model of oscillatory Ca(2+) waves based on experimental data that incorporate both the inositol trisphosphate receptor and the ryanodine receptor. We then combined this Ca(2+) model and our modified actin-myosin cross-bridge model to investigate the role and contribution of oscillatory Ca(2+) waves to contractile force generation in mouse ASMCs. The model predicts that: 1), the difference in behavior of agonist- and KCl-induced Ca(2+) waves results principally from the fact that the sarcoplasmic reticulum is depleted during agonist-induced oscillations, but is overfilled during KCl-induced oscillations; 2), regardless of the order in which agonist and KCl are added into the cell, the resulting [Ca(2+)](i) oscillations will always be the short-period, agonist-induced-like oscillations; and 3), both the inositol trisphosphate receptor and the ryanodine receptor densities are higher toward one end of the cell. In addition, our results indicate that oscillatory Ca(2+) waves generate less contraction than whole-cell Ca(2+) oscillations induced by the same agonist concentration. This is due to the spatial inhomogeneity of the receptor distributions.
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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.