ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Pancreatic β-cell Na+ channels control global Ca2+ signaling and oxidative metabolism by inducing Na+ and Ca2+ responses that are propagated into mitochondria.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 55 citations in OpenAlex.
- Sodium accumulation in breast cancer predicts malignancy and treatment response.British journal of cancer · 2022Trial
- Diuretics: a review of the pharmacology and effects on glucose homeostasis.Frontiers in pharmacology · 2025Review
- Mitochondrial sodium/calcium exchanger NCLX regulates glycolysis in astrocytes, impacting on cognitive performance.Journal of neurochemistry · 2023Article
- Mitochondrial signal transduction.Cell metabolism · 2022Review
- Mitochondrial Metal Ion Transport in Cell Metabolism and Disease.International journal of molecular sciences · 2021Review
- Aberrant activity of mitochondrial NCLX is linked to impaired synaptic transmission and is associated with mental retardation.Communications biology · 2021Article
- Distinct properties of CaCell calcium · 2021Article
- Mitochondrial Calcium Signaling in Pancreatic β-Cell.International journal of molecular sciences · 2021Review
- Structural and Functional Characterization of a NaCirculation research · 2021Article
- Management of mitochondrial diabetes in the era of novel therapies.Journal of diabetes and its complications · 2021Article
- NCLX prevents cell death during adrenergic activation of the brown adipose tissue.Nature communications · 2020Article
- Membrane current evoked by mitochondrial NaThe journal of physiological sciences : JPS · 2020Article
- Quantitative determination of cellular [NaThe Journal of general physiology · 2019Article
- The association of calcium channel blockers with β-cell function in type 2 diabetic patients: A cross-sectional study.Journal of clinical hypertension (Greenwich, Conn.) · 2019Article
- Mitochondrial calcium signalling and neurodegenerative diseases.Neuronal signaling · 2018Review
- Crosslink between calcium and sodium signalling.Experimental physiology · 2018Review
- Mitochondrial Calcium Dysregulation Contributes to Dendrite Degeneration Mediated by PD/LBD-Associated LRRK2 Mutants.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Optogenetic control of mitochondrial metabolism and CaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mitochondria control store-operated CaThe EMBO journal · 2017Article
- Roles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic Neuropathy.International journal of molecular sciences · 2016Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Communication between the plasma membrane and mitochondria is essential for initiating the Ca(2+) and metabolic signals required for secretion in β cells. Although voltage-dependent Na(+) channels are abundantly expressed in β cells and activated by glucose, their role in communicating with mitochondria is unresolved. Here, we combined fluorescent Na(+), Ca(2+), and ATP imaging, electrophysiological analysis with tetrodotoxin (TTX)-dependent block of the Na(+) channel, and molecular manipulation of mitochondrial Ca(2+) transporters to study the communication between Na(+) channels and mitochondria. We show that TTX inhibits glucose-dependent depolarization and blocks cytosolic Na(+) and Ca(2+) responses and their propagation into mitochondria. TTX-sensitive mitochondrial Ca(2+) influx was largely blocked by knockdown of the mitochondrial Ca(2+) uniporter (MCU) expression. Knockdown of the mitochondrial Na(+)/Ca(2+) exchanger (NCLX) and Na(+) dose response analysis demonstrated that NCLX mediates the mitochondrial Na(+) influx and is tuned to sense the TTX-sensitive cytosolic Na(+) responses. Finally, TTX blocked glucose-dependent mitochondrial Ca(2+) rise, mitochondrial metabolic activity, and ATP production. Our results show that communication of the Na(+) channels with mitochondria shape both global Ca(2+) and metabolism signals linked to insulin secretion in β cells.- Nita, I. I., Hershfinkel, M., Kantor, C., Rutter, G. A., Lewis, E. C., Sekler, I. Pancreatic β-cell Na(+) channels control global Ca(2+) signaling and oxidative metabolism by inducing Na(+) and Ca(2+) responses that are propagated into mitochondria.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.