ArticleThe Journal of biological chemistry2010
Mitochondrial Ca2+ uptake increases Ca2+ release from inositol 1,4,5-trisphosphate receptor clusters in smooth muscle cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- CaPhysiological reviews · 2024Review
- Sex-Specific Differences in Endothelial Function Are Driven by Divergent Mitochondrial CaJournal of the American Heart Association · 2022Article
- The relevance of organelle interactions in cellular senescence.Theranostics · 2022Review
- Carbenoxolone and 18β-glycyrrhetinic acid inhibit inositol 1,4,5-trisphosphate-mediated endothelial cell calcium signalling and depolarise mitochondria.British journal of pharmacology · 2021Article
- Hydrogen peroxide depolarizes mitochondria and inhibits IPCell calcium · 2019Article
- Modeling the role of endoplasmic reticulum-mitochondria microdomains in calcium dynamics.Scientific reports · 2019Article
- Increased Vascular Contractility in Hypertension Results From Impaired Endothelial Calcium Signaling.Hypertension (Dallas, Tex. : 1979) · 2019Article
- Mitochondrial ATP production provides long-range control of endothelial inositol trisphosphate-evoked calcium signaling.The Journal of biological chemistry · 2019Article
- Spatially structured cell populations process multiple sensory signals in parallel in intact vascular endothelium.Science signaling · 2018Article
- The effects of mitochondrial inhibitors on CaCell calcium · 2018Article
- The Endothelium Solves Problems That Endothelial Cells Do Not Know Exist.Trends in pharmacological sciences · 2017Review
- The Mitochondrial CaHandbook of experimental pharmacology · 2017Review
- Calcium Channels in Vascular Smooth Muscle.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Endoplasmic reticulum-mediated signalling in cellular microdomains.Acta physiologica (Oxford, England) · 2017Review
- Age decreases mitochondrial motility and increases mitochondrial size in vascular smooth muscle.The Journal of physiology · 2016Article
- Pressure-dependent regulation of Ca2+ signalling in the vascular endothelium.The Journal of physiology · 2015Article
- The role of Ca(2+) influx in spontaneous Ca(2+) wave propagation in interstitial cells of Cajal from the rabbit urethra.The Journal of physiology · 2015Article
- Optimal microdomain crosstalk between endoplasmic reticulum and mitochondria for Ca2+ oscillations.Scientific reports · 2015Article
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Smooth muscle activities are regulated by inositol 1,4,5-trisphosphate (InsP(3))-mediated increases in cytosolic Ca2+ concentration ([Ca2+](c)). Local Ca2+ release from an InsP(3) receptor (InsP(3)R) cluster present on the sarcoplasmic reticulum is termed a Ca2+ puff. Ca2+ released via InsP(3)R may diffuse to adjacent clusters to trigger further release and generate a cell-wide (global) Ca2+ rise. In smooth muscle, mitochondrial Ca2+ uptake maintains global InsP(3)-mediated Ca2+ release by preventing a negative feedback effect of high [Ca2+] on InsP(3)R. Mitochondria may regulate InsP(3)-mediated Ca2+ signals by operating between or within InsP(3)R clusters. In the former mitochondria could regulate only global Ca2+ signals, whereas in the latter both local and global signals would be affected. Here whether mitochondria maintain InsP(3)-mediated Ca2+ release by operating within (local) or between (global) InsP(3)R clusters has been addressed. Ca2+ puffs evoked by localized photolysis of InsP(3) in single voltage-clamped colonic smooth muscle cells had amplitudes of 0.5-4.0 F/F(0), durations of approximately 112 ms at half-maximum amplitude, and were abolished by the InsP(3)R inhibitor 2-aminoethoxydiphenyl borate. The protonophore carbonyl cyanide 3-chloropheylhydrazone and complex I inhibitor rotenone each depolarized DeltaPsi(M) to prevent mitochondrial Ca2+ uptake and attenuated Ca2+ puffs by approximately 66 or approximately 60%, respectively. The mitochondrial uniporter inhibitor, RU360, attenuated Ca2+ puffs by approximately 62%. The "fast" Ca2+ chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acted like mitochondria to prolong InsP(3)-mediated Ca2+ release suggesting that mitochondrial influence is via their Ca2+ uptake facility. These results indicate Ca2+ uptake occurs quickly enough to influence InsP(3)R communication at the intra-cluster level and that mitochondria regulate both local and global InsP(3)-mediated Ca2+ signals.
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