ArticleThe Biochemical journal2000
Inositol 1,4,5-trisphosphate-induced Ca2+ release is inhibited by mitochondrial depolarization.
Article in The Biochemical journal, 2000. 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, 73 citations in OpenAlex.
- Mitochondria regulate inositol triphosphate-mediated CaThe Journal of physiology · 2025Article
- TRPM8 channel inhibitor-encapsulated hydrogel as a tunable surface for bone tissue engineering.Scientific reports · 2021Article
- Mitochondrial Dysfunction and Calcium Dysregulation in Leigh Syndrome Induced Pluripotent Stem Cell Derived Neurons.International journal of molecular sciences · 2020Article
- Hydrogen peroxide depolarizes mitochondria and inhibits IPCell calcium · 2019Article
- Mitochondrial ATP production provides long-range control of endothelial inositol trisphosphate-evoked calcium signaling.The Journal of biological chemistry · 2019Article
- Endothelial mitochondria regulate the intracellular Ca2+ response to fluid shear stress.American journal of physiology. Cell physiology · 2016Article
- Interaction between endoplasmic/sarcoplasmic reticulum stress (ER/SR stress), mitochondrial signaling and Ca(2+) regulation in airway smooth muscle (ASM).Canadian journal of physiology and pharmacology · 2015Review
- Hypoxia-induced changes in Ca(2+) mobilization and protein phosphorylation implicated in impaired wound healing.American journal of physiology. Cell physiology · 2014Article
- Examining the role of mitochondria in Ca²⁺ signaling in native vascular smooth muscle.Microcirculation (New York, N.Y. : 1994) · 2013Review
- Effects of mitochondrial uncoupling on Ca(2+) signaling during excitation-contraction coupling in atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2013Article
- Inflammation alters regional mitochondrial Ca²+ in human airway smooth muscle cells.American journal of physiology. Cell physiology · 2012Article
- Measuring mitochondrial function in intact cardiac myocytes.Journal of molecular and cellular cardiology · 2012Review
- Mitochondrial Ca2+ uptake increases Ca2+ release from inositol 1,4,5-trisphosphate receptor clusters in smooth muscle cells.The Journal of biological chemistry · 2010Article
- Inhibitors of cellular signalling are cytotoxic or block the budded-to-hyphal transition in the pathogenic yeast Candida albicans.Journal of medical microbiology · 2009Article
- Differential effects of methionine and cysteine oxidation on [Ca2+] i in cultured hippocampal neurons.Cellular and molecular neurobiology · 2009Article
- Mitochondria modulate Ca2+-dependent glutamate release from rat cortical astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- The use of CalciumOrange-5N as a specific marker of mitochondrial Ca2+ in mouse skeletal muscle fibers.Pflugers Archiv : European journal of physiology · 2008Article
- A homozygous mutation in a novel zinc-finger protein, ERIS, is responsible for Wolfram syndrome 2.American journal of human genetics · 2007 · on this mapArticle
- Inositol 1,3,4,5-tetrakisphosphate negatively regulates phosphatidylinositol-3,4,5- trisphosphate signaling in neutrophils.Immunity · 2007Article
- The plasma membrane Na+/Ca2+ exchange inhibitor KB-R7943 is also a potent inhibitor of the mitochondrial Ca2+ uniporter.British journal of pharmacology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the consequences of depolarizing the mitochondrial membrane potential (Deltapsi(mit)) on Ca(2+) signals arising via inositol 1,4,5-trisphosphate receptors (InsP(3)R) in hormone-stimulated HeLa cells. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) or a mixture of antimycin A+oligomycin were found to rapidly depolarize Deltapsi(mit). Mitochondrial depolarization enhanced the number of cells responding to a brief application of a Ca(2+)-mobilizing hormone and prolonged the recovery of cytosolic Ca(2+) after washout of the hormone; effects consistent with the removal of a passive Ca(2+) buffer. However, with repeated application of the same hormone concentration both the number of responsive cells and peak Ca(2+) changes were observed to progressively decline. The inhibition of Ca(2+) signalling was observed using different Ca(2+)-mobilizing hormones and also with a membrane-permeant Ins(1,4,5)P(3) ester. Upon washout of FCCP, the Ca(2+) signals recovered with a time course similar to the re-establishment of Deltapsi(mit). Global measurements indicated that none of the obvious factors such as changes in pH, ATP concentration, cellular redox state, permeability transition pore activation or reduction in Ca(2+)-store loading appeared to underlie the inhibition of Ca(2+) signalling. We therefore suggest that local changes in one or more of these factors, as a consequence of depolarizing Deltapsi(mit), prevents InsP(3)R activation.
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