ArticleProceedings of the National Academy of Sciences of the United States of America2007
TRPM7 channels in hippocampal neurons detect levels of extracellular divalent cations.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 105 citations in OpenAlex.
- Trial
- Ischemia-Reperfusion Increases TRPM7 Expression in Mouse Retinas.International journal of molecular sciences · 2023Article
- Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel.Frontiers in cell and developmental biology · 2021Article
- Transcriptomic Profiling of Ca2+ Transport Systems During the Formation of the Cerebral Cortex in Mice.Cells · 2020Article
- Neuroprotective Effects of AG490 in Neonatal Hypoxic-Ischemic Brain Injury.Molecular neurobiology · 2019Article
- Leptin Induces Hypertension Acting on Transient Receptor Potential Melastatin 7 Channel in the Carotid Body.Circulation research · 2019Article
- Role of the chanzyme TRPM7 in the nervous system in health and disease.Cellular and molecular life sciences : CMLS · 2019Review
- Opening TRPP2 (Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Modulation of MgThe journal of physiological sciences : JPS · 2019Article
- The kinase activity of the channel-kinase protein TRPM7 regulates stability and localization of the TRPM7 channel in polarized epithelial cells.The Journal of biological chemistry · 2018Article
- The Different Facets of Extracellular Calcium Sensors: Old and New Concepts in Calcium-Sensing Receptor Signalling and Pharmacology.International journal of molecular sciences · 2018Review
- TRPM7 is a unique target for therapeutic intervention of stroke.International journal of physiology, pathophysiology and pharmacology · 2017Review
- Neuroprotective Role of MicroRNA-22 in a 6-Hydroxydopamine-Induced Cell Model of Parkinson's Disease via Regulation of Its Target Gene TRPM7.Journal of molecular neuroscience : MN · 2016Article
- Function and regulation of TRPM7, as well as intracellular magnesium content, are altered in cells expressing ΔF508-CFTR and G551D-CFTR.Cellular and molecular life sciences : CMLS · 2016Article
- TRPM7 is a molecular substrate of ATP-evoked P2X7-like currents in tumor cells.The Journal of general physiology · 2016Article
- TRPM7 Regulates Axonal Outgrowth and Maturation of Primary Hippocampal Neurons.Molecular neurobiology · 2016Article
- Long-Term Estrogen Receptor Beta Agonist Treatment Modifies the Hippocampal Transcriptome in Middle-Aged Ovariectomized Rats.Frontiers in cellular neuroscience · 2016Article
- Article
- Redox-sensitive transient receptor potential channels in oxygen sensing and adaptation.Pflugers Archiv : European journal of physiology · 2016Review
- Curcumin as a double-edged sword for stem cells: dose, time and cell type-specific responses to curcumin.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2015Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to low Ca(2+) and/or Mg(2+) is tolerated by cardiac myocytes, astrocytes, and neurons, but restoration to normal divalent cation levels paradoxically causes Ca(2+) overload and cell death. This phenomenon has been called the "Ca(2+) paradox" of ischemia-reperfusion. The mechanism by which a decrease in extracellular Ca(2+) and Mg(2+) is "detected" and triggers subsequent cell death is unknown. Transient periods of brain ischemia are characterized by substantial decreases in extracellular Ca(2+) and Mg(2+) that mimic the initial condition of the Ca(2+) paradox. In CA1 hippocampal neurons, lowering extracellular divalents stimulates a nonselective cation current. We show that this current resembles TRPM7 currents in several ways. Both (i) respond to transient decreases in extracellular divalents with inward currents and cell excitation, (ii) demonstrate outward rectification that depends on the presence of extracellular divalents, (iii) are inhibited by physiological concentrations of intracellular Mg(2+), (iv) are enhanced by intracellular phosphatidylinositol 4,5-bisphosphate (PIP(2)), and (v) can be inhibited by Galphaq-linked G protein-coupled receptors linked to phospholipase C beta1-induced hydrolysis of PIP(2). Furthermore, suppression of TRPM7 expression in hippocampal neurons strongly depressed the inward currents evoked by lowering extracellular divalents. Finally, we show that activation of TRPM7 channels by lowering divalents significantly contributes to cell death. Together, the results demonstrate that TRPM7 contributes to the mechanism by which hippocampal neurons "detect" reductions in extracellular divalents and provide a means by which TRPM7 contributes to neuronal death during transient brain 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.