Modeling a novel mechanism of calcium-induced calcium release in vascular smooth muscle cell
Date
2012
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Abstract
Recent work has revealed a microdomain m cerebral arterial smooth muscle comprised of caveolae and the sarcoplasmic reticulum. Immunolabeling techniques indicate that T-type Ca2+ channels (Cav3.2) and ryanodine receptors localize to this microdomain while L-type Ca2+ channels do not. Based on these observations, we hypothesize that T-type Ca2+ channels play a major role in triggering RyR receptors and consequently in modulating Ca2+ sparks. To address this hypothesis, we developed a detailed tissue-specific biophysical model that can simulate several aspects of Ca2+ sparks in cerebral arterial SMCs by integrating independent formulations of cellular components with different sets of parameter adjustments. The simulation results show that the Calcium Induced Calcium Release (CICR) process can be initiated in a virtual microdomain containing Cav3.2 and RyR channels. These CICR events are repetitive and voltage dependent in that higher depolarization lead to higher CICR frequencies.
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Bibliography: p. 69-72
Many pages are in colour.
Includes copy of copyright permissions. Original copies with original Partial Copyright Licence.
Many pages are in colour.
Includes copy of copyright permissions. Original copies with original Partial Copyright Licence.
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Bigdely Shamloo, K. (2012). Modeling a novel mechanism of calcium-induced calcium release in vascular smooth muscle cell (Master's thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/4963