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Evidence for mitochondrial Ca(2+)-induced Ca2+ release in permeabilised endothelial cells.
Biochem Biophys Res Commun. 1998 May 19; 246(2):543-8.BB

Abstract

Generally most intracellular Ca2+ is stored in the endoplasmic reticulum (ER) and mitochondria. Recently a mitochondrial Ca(2+)-induced Ca2+ release (mCICR) mechanism, unconnected with ryanodine receptors (RyR's), has been shown in tumour cells. The existence of a mitochondrial Ca2+ release mechanism in BAE cells was investigated using saponin-permeabilised BAE cells. When buffered intracellular solution were 'stepped' from 10 nM to 10 microM free Ca2+, the mitochondrial inhibitors CN (2 mM), FCCP (1 microM), and RR (20 microM) significantly reduced total CICR by approximately 25%. The ER Ca(2+)-ATPase inhibitor thapsigargin (100 nM) had no effect. Furthermore, cyclosporin A (200 nM), an inhibitor of the mitochondrial permeability transition pore (PTP), abolished total CICR. Therefore, the novel ryanodine-caffeine insensitive CICR mechanism previously reported in BAE cells involves mitochondrial Ca2 release. It is proposed that in BAE cells, mCICR occurs via the mitochondrial PTP and may be physiologically important in endothelial cell Ca2+ signalling.

Authors+Show Affiliations

Department of Physiological Sciences, Medical School, Newcastle University, Newcastle upon Tyne, United Kingdom. P.G.Wood@newcastle.ac.ukNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9610399

Citation

Wood, P G., and J I. Gillespie. "Evidence for Mitochondrial Ca(2+)-induced Ca2+ Release in Permeabilised Endothelial Cells." Biochemical and Biophysical Research Communications, vol. 246, no. 2, 1998, pp. 543-8.
Wood PG, Gillespie JI. Evidence for mitochondrial Ca(2+)-induced Ca2+ release in permeabilised endothelial cells. Biochem Biophys Res Commun. 1998;246(2):543-8.
Wood, P. G., & Gillespie, J. I. (1998). Evidence for mitochondrial Ca(2+)-induced Ca2+ release in permeabilised endothelial cells. Biochemical and Biophysical Research Communications, 246(2), 543-8.
Wood PG, Gillespie JI. Evidence for Mitochondrial Ca(2+)-induced Ca2+ Release in Permeabilised Endothelial Cells. Biochem Biophys Res Commun. 1998 May 19;246(2):543-8. PubMed PMID: 9610399.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evidence for mitochondrial Ca(2+)-induced Ca2+ release in permeabilised endothelial cells. AU - Wood,P G, AU - Gillespie,J I, PY - 1998/6/4/pubmed PY - 1998/6/4/medline PY - 1998/6/4/entrez SP - 543 EP - 8 JF - Biochemical and biophysical research communications JO - Biochem Biophys Res Commun VL - 246 IS - 2 N2 - Generally most intracellular Ca2+ is stored in the endoplasmic reticulum (ER) and mitochondria. Recently a mitochondrial Ca(2+)-induced Ca2+ release (mCICR) mechanism, unconnected with ryanodine receptors (RyR's), has been shown in tumour cells. The existence of a mitochondrial Ca2+ release mechanism in BAE cells was investigated using saponin-permeabilised BAE cells. When buffered intracellular solution were 'stepped' from 10 nM to 10 microM free Ca2+, the mitochondrial inhibitors CN (2 mM), FCCP (1 microM), and RR (20 microM) significantly reduced total CICR by approximately 25%. The ER Ca(2+)-ATPase inhibitor thapsigargin (100 nM) had no effect. Furthermore, cyclosporin A (200 nM), an inhibitor of the mitochondrial permeability transition pore (PTP), abolished total CICR. Therefore, the novel ryanodine-caffeine insensitive CICR mechanism previously reported in BAE cells involves mitochondrial Ca2 release. It is proposed that in BAE cells, mCICR occurs via the mitochondrial PTP and may be physiologically important in endothelial cell Ca2+ signalling. SN - 0006-291X UR - https://www.unboundmedicine.com/medline/citation/9610399/Evidence_for_mitochondrial_Ca_2+__induced_Ca2+_release_in_permeabilised_endothelial_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(98)98661-2 DB - PRIME DP - Unbound Medicine ER -