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The Strathprints institutional repository is a digital archive of University of Strathclyde's Open Access research outputs. Strathprints provides access to thousands of Open Access research papers by University of Strathclyde researchers, including by researchers from the Department of Computer & Information Sciences involved in mathematically structured programming, similarity and metric search, computer security, software systems, combinatronics and digital health.

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Mitochondrial regulation of cytosolic Ca2+ signals in smooth muscle

McCarron, John and Olson, Marnie and Chalmers, Susan (2012) Mitochondrial regulation of cytosolic Ca2+ signals in smooth muscle. Pflügers Archiv European Journal of Physiology, 464 (specia). pp. 51-62.

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Abstract

The cytosolic Ca2+ concentration ([Ca2+]c) controls virtually every activity of smooth muscle, including contraction, migration, transcription, division and apoptosis. These processes may be activated by large (>10 μM) amplitude [Ca2+]c increases, which occur in small restricted regions of the cell or by smaller (<1 μM) amplitude changes throughout the bulk cytoplasm. Mitochondria contribute to the regulation of these signals by taking up Ca2+. However, mitochondria’s reported low affinity for Ca2+ is thought to require the organelle to be positioned close to ion channels and within a microdomain of high [Ca2+]. In cultured smooth muscle, mitochondria are highly dynamic structures but in native smooth muscle mitochondria are immobile, apparently strategically positioned organelles that regulate the upstroke and amplitude of IP3-evoked Ca2+ signals and IP3 receptor (IP3R) cluster activity. These observations suggest mitochondria are positioned within the high [Ca2+] microdomain arising from an IP3R cluster to exert significant local control of channel activity. On the other hand, neither the upstroke nor amplitude of voltage-dependent Ca2+ entry is modulated by mitochondria; rather, it is the declining phase of the transient that is regulated by the organelle. Control of the declining phase of the transient requires a high mitochondrial affinity for Ca2+ to enable uptake to occur over the normal physiological Ca2+ range (<1 μM). Thus, in smooth muscle, mitochondria regulate Ca2+ signals exerting effects over a large range of [Ca2+] (∼200 nM to at least tens of micromolar) to provide a wide dynamic range in the control of Ca2+ signals.