ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
A critical role for the potassium-dependent sodium-calcium exchanger NCKX2 in protection against focal ischemic brain damage.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- miR135a administration ameliorates brain ischemic damage by preventing TRPM7 activation during brain ischemia.CNS neuroscience & therapeutics · 2024Article
- Regulation of KInternational journal of molecular sciences · 2022Review
- KInternational journal of molecular sciences · 2022Article
- Ligands of the Neuropeptide Y Y2 Receptors as a Potential Multitarget Therapeutic Approach for the Protection of the Neurovascular Unit Against Acute Ischemia/Reperfusion: View from the Perspective of the Laboratory Bench.Translational stroke research · 2022Review
- Anti-miR-223-5p Ameliorates Ischemic Damage and Improves Neurological Function by Preventing NCKX2 Downregulation after Ischemia in Rats.Molecular therapy. Nucleic acids · 2019Article
- A Genome-Wide Analysis of the Penumbral Volume in Inbred Mice following Middle Cerebral Artery Occlusion.Scientific reports · 2019Article
- Tocotrienol Rich Fraction Supplementation Modulate Brain Hippocampal Gene Expression in APPswe/PS1dE9 Alzheimer's Disease Mouse Model.Journal of Alzheimer's disease : JAD · 2019Article
- Synergistic Association of Valproate and Resveratrol Reduces Brain Injury in Ischemic Stroke.International journal of molecular sciences · 2018Article
- Genetic Effects on the Correlation Structure of CVD Risk Factors: Exome-Wide Data From a Ghanaian Population.Global heart · 2017Review
- Neuronal NCX1 overexpression induces stroke resistance while knockout induces vulnerability via Akt.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- The role of Na+/Ca2+ exchanger subtypes in neuronal ischemic injury.Translational stroke research · 2015Review
- Ionic regulation of cell volume changes and cell death after ischemic stroke.Translational stroke research · 2014Review
- Endocytosis of somatodendritic NCKX2 is regulated by Src family kinase-dependent tyrosine phosphorylation.Frontiers in cellular neuroscience · 2013Article
- Article
- Transient filament occlusion of the middle cerebral artery in rats: does the reperfusion method matter 24 hours after perfusion?BMC neuroscience · 2012Article
- KIF21A-mediated axonal transport and selective endocytosis underlie the polarized targeting of NCKX2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Residues contributing to the Na(+)-binding pocket of the SLC24 Na(+)/Ca(2+)-K(+) Exchanger NCKX2.The Journal of biological chemistry · 2010Article
- Ionic storm in hypoxic/ischemic stress: can opioid receptors subside it?Progress in neurobiology · 2010Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The superfamily of cation/Ca2+ plasma-membrane exchangers contains two branches, the K+-independent Na+-Ca2+ exchangers (NCXs) and the K+-dependent Na+-Ca2+ exchangers (NCKXs), widely expressed in mammals. NCKX2 is the major neuronally expressed isoform among NCKX members. Despite its importance in maintaining Na+, Ca2+, and K+ homeostasis in the CNS, the role of NCKX2 during cerebral ischemia, a condition characterized by an alteration of ionic concentrations, has not yet been investigated. The present study examines NCKX2 role in the development of ischemic brain damage in permanent middle cerebral artery occlusion (pMCAO) and transient middle cerebral artery occlusion. Furthermore, to evaluate the effect of nckx2 ablation on neuronal survival, nckx2-/- primary cortical neurons were subjected to oxygen glucose deprivation plus reoxygenation. NCKX2 mRNA and protein expression was evaluated in the ischemic core and surrounding ipsilesional areas, at different time points after pMCAO in rats. In ischemic core and in periinfarctual area, NCKX2 mRNA and protein expression were downregulated. In addition, NCKX2 knock-down by antisense oligodeoxynucleotide and NCKX2 knock-out by genetic disruption dramatically increased infarct volume. Accordingly, nckx2-/- primary cortical neurons displayed a higher vulnerability and a greater [Ca2+]i increase under hypoxic conditions, compared with nckx2+/+ neurons. In addition, NCKX currents both in the forward and reverse mode of operation were significantly reduced in nckx2-/- neurons compared with nckx2+/+ cells. Overall, these results indicate that NCKX2 is involved in brain ischemia, and it may represent a new potential target to be investigated in the study of the molecular mechanisms involved in cerebral ischemia.
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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 OpenQuestion graph.