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Life after the birth of the mitochondrial Na^+/Ca^(2+) exchanger,NCLX

Science China(Life Sciences) 2015年第1期58卷 59-65页

作者： NITA Lulia I. HERSHFINKEL Michal sekler israel Department of Physiology and Cell Biology Faculty of Health SciencesBen-Gurion University of the Negev

Powered by the mitochondrial membrane potential,Ca2+ permeates the mitochondria via a Ca2+ channel termed Ca2+ uniporter and is pumped out by a Na+/Ca2+ exchanger,both of which are located on the inner mitochondrial *** Ca2+ transients are critical for metabolic activity and regulating global Ca2+ *** the other hand,failure to control mitochondrial Ca2+ is a hallmark of ischemic and neurodegenerative *** their importance,identifying the uniporter and exchanger remains elusive and their inhibitors are *** review will focus on the mitochondrial exchanger,initially describing how it was molecularly identified and linked to a novel member of the Na+/Ca2+ exchanger superfamily termed *** control of NCLX expression provides a selective tool to determine its physiological role in a variety of cell *** lymphocytes,NCLX is essential for refilling the endoplasmic reticulum Ca2+ stores required for antigen-dependent *** of NCLX with the store-operated channel in astroglia controls Ca2+ influx and thereby neuro-transmitter release and cell *** refilling of the Ca2+ stores in the sarcoplasmic reticulum,which is controlled by NCLX,determines the frequency of action potential and Ca2+ transients in *** is emerging as a hub for integrating glucose-dependent Na+ and Ca2+ signaling in pancreatic β cells,and the specific molecular control of NCLX expression resolved the controversy regarding its role in neurons and β *** studies on an NCLX knockdown mouse model and identification of human NCLX mutations are expected to determine the role of mitochondrial Ca2+ efflux in organ activity and whether NCLX inactivation is linked to ischemic and/or neurodegenerative ***-function analysis and protein analysis will identify the NCLX mode of regulation and its partners in the inner membrane of the mitochondria.

关键词： NCLX MCU mitochondrial Ca^2+ signaling Na^+/Ca^2+ exchanger Na+ signaling

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ASIC1a channel modulates mitochondrial energy metabolism in mouse cortical neurons

ASIC1a channel modulates mitochondrial energy metabolism in ...

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中国神经科学学会第十二届全国学术会议

作者： Fan Liu Ivana Savic Qin Hu israel sekler Tian-Le Xu Discipline of Neuroscience and Department of Anatomy Histology and EmbryologyShanghai Jiao Tong University School of Medicine Department of Physiology and Cell Biology Faculty of Health Sciences Ben-Gurion University of the Negev

Acid-sensing ion channel 1 a(ASIC1 a) is involved in synaptic plasticity, learning/memory and ischemic neuronal death. Recently, we demonstrated that ASIC1 a proteins are present in the mitochondria of mouse cortical neurons and closely related to reactive oxygen species(ROS) generation. Mitochondria are popularly known as the powerhouse of the cell, therefore we aimed to investigate the function of ASIC1 a in neuronal energy metabolism. We found that deletion of ASIC1 a gene causes significant decrease of basal respiration, maximal respiration as well as ATP production in cultured neurons, indicating impaired mitochondrial metabolic function. Furthermore, we observed the reduction of NAD, induction of mitochondrial permeability transition pore, and increased ROS production in ASIC1 a KO neurons. All these results supported that lose of ASIC1 a results in worse energy metabolism and consequently more severe oxidative stress. Moreover, extracellular acidosis dramatically increases mitochondrial calcium in WT neurons but not in ASIC1 a KO neurons, and the increased mitochondrial calcium depends on the plasma membrane ASIC1 a channels. As mitochondrial calcium is an important modulator of the Krebs cycle, electron transport chain and FFATP synthase, the suppressed energy metabolism may be a causative event of reduced mitochondrial calcium in ASIC1 a KO neurons. Our data suggest that ASIC1 a may modulate energy metabolism through increasing mitochondrial calcium.

关键词： ASIC1a Mitochondrial calcium Energy metabolism

来源： cnki会议评论