The mitochondrial Na+/Ca2+ exchanger-NCLX is an integrating hub for glucose dependent Na+ and Ca2+ signaling in pancreatic $β$ cells Academic Article uri icon

abstract

  • Although Na+ channels are abundantly expressed in β cells how Na+ fluxes are linked to glucose dependent Ca 2+ signaling linked to pancreatic secretion is poorly underwood. Here we addressed the role of Na+ influx in regulating glucose dependent mitochondrial Ca 2+ shuttling and cytosolic Ca 2+ transients by fluorescently monitoring cytosolic and mitochondrial Na+ and Ca 2+ transport in pancreatic b cells. Influx of Na+ via the TTX sensitive channels activated the mitochondrial Na+/Ca 2+ exchanger NCLX, which in turn stimulated glucose dependent cytosolic Ca 2+ influx. This effect was mimicked by pretreating cells with ouabain that by triggering cytosolic Na+ accumulation eliminated the TTX dependent inhibition of mitochondrial and cytosolic Ca 2+ signaling. Importantly knock down of NCLX expression by siNCLX eliminated the stimulatory effects of ouabain. Our …

publication date

  • January 1, 2013