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.
Описание
A mathematical analysis of agonist- and KCl-induce... [Biophys J. 2010] - PubMed - NCBI
%0 Journal Article
%1 Wang:2010:Biophys-J:20371316
%A Wang, I Y
%A Bai, Y
%A Sanderson, M J
%A Sneyd, J
%D 2010
%E Journal, Biophysical
%J Biophys J
%K airway calcium cell mathematical model muscle smooth
%N 7
%P 1170-1181
%R 10.1016/j.bpj.2009.12.4273
%T A mathematical analysis of agonist- and KCl-induced Ca(2+) oscillations in mouse airway smooth muscle cells
%U http://www.ncbi.nlm.nih.gov/pubmed/20371316
%V 98
%X 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.
@article{Wang:2010:Biophys-J:20371316,
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.},
added-at = {2012-03-02T10:32:12.000+0100},
author = {Wang, I Y and Bai, Y and Sanderson, M J and Sneyd, J},
biburl = {https://www.bibsonomy.org/bibtex/26a5b2fbdfbe619f5da274537c4f2e757/huguette},
description = {A mathematical analysis of agonist- and KCl-induce... [Biophys J. 2010] - PubMed - NCBI},
doi = {10.1016/j.bpj.2009.12.4273},
editor = {Journal, Biophysical},
interhash = {c9e388c87eb97259d7badbbb7f5a2153},
intrahash = {6a5b2fbdfbe619f5da274537c4f2e757},
journal = {Biophys J},
keywords = {airway calcium cell mathematical model muscle smooth},
month = apr,
number = 7,
pages = {1170-1181},
pmid = {20371316},
timestamp = {2012-03-02T10:32:12.000+0100},
title = {A mathematical analysis of agonist- and KCl-induced Ca(2+) oscillations in mouse airway smooth muscle cells},
url = {http://www.ncbi.nlm.nih.gov/pubmed/20371316},
volume = 98,
year = 2010
}