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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/116833
Título

The coupling of plasma membrane calcium entry to calcium uptake by endoplasmic reticulum and mitochondria

AutorGarcía-Sancho, Javier
Fecha de publicación2014
EditorPhysiological Society (Great Britain)
John Wiley & Sons
CitaciónJournal of Physiology 592(2): 261-268 (2014)
ResumenKey points: Cross-talk between organelles and plasma membrane Ca2+ channels modulates cytosolic Ca2+ signals in different ways. In chromaffin cells Ca2+ entry through voltage-operated channels is amplified by Ca2+ release from the endoplasmic reticulum (ER) and generates subplasmalemmal high Ca2+ microdomains (HCMDs) as high as 20-50 μm, which trigger exocytosis. Subplasmalemmal mitochondria take up Ca2+ from HCMDs and avoid progression of the Ca2+ wave towards the cell core. In non-excitable HEK293 cells activation of store-operated Ca2+ entry triggered by ER Ca2+ emptying also generates subplasmalemmal HCMDs of about 2 μm. In this case most of the Ca2+ is taken up by the ER rather than by mitochondria. This outcome may be explained because sarco-endoplasmic reticulum Ca2+ ATPase (SERCA) has much higher Ca2+ affinity than mitochondria. The relative positioning of organelles, channels and accessory proteins may also play a role. Cross-talk between organelles and plasma membrane Ca2+ channels is essential for modulation of the cytosolic Ca2+ ([Ca2+]C) signals, but such modulation may differ among cells. In chromaffin cells Ca2+ entry through voltage-operated channels induces calcium release from the endoplasmic reticulum (ER) that amplifies the signal. [Ca2+]C microdomains as high as 20-50 μm are sensed by subplasmalemmal mitochondria, which accumulate large amounts of Ca2+ through the mitochondrial Ca2+ uniporter (MCU). Mitochondria confine the high-Ca2+ microdomains (HCMDs) to beneath the plasma membrane, where exocytosis of secretory vesicles happens. Cell core [Ca2+]C is much smaller (1-2 μm). By acting as a Ca2+ sink, mitochondria stabilise the HCMD in space and time. In non-excitable HEK293 cells, activation of store-operated Ca2+ entry, triggered by ER Ca2+ emptying, also generated subplasmalemmal HCMDs, but, in this case, most of the Ca2+ was taken up by the ER rather than by mitochondria. The smaller size of the [Ca2+]C peak in this case (about 2 μm) may contribute to this outcome, as the sarco-endoplasmic reticulum Ca2+ ATPase has much higher Ca2+ affinity than MCU. It is also possible that the relative positioning of organelles, channels and effectors, as well as cytoskeleton and accessory proteins plays an important role. © 2013 The Physiological Society.
URIhttp://hdl.handle.net/10261/116833
DOI10.1113/jphysiol.2013.255661
Identificadoresdoi: 10.1113/jphysiol.2013.255661
issn: 0022-3751
e-issn: 1469-7793
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