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Mitochondrial regulation of sarcoplasmic reticulum Ca2+ content in vascular smooth muscle cells.
Circ Res. 2009 Jan 02; 104(1):104-12.CircR

Abstract

Subplasmalemmal ion fluxes have global effects on Ca(2+) signaling in vascular smooth muscle. Measuring cytoplasmic and mitochondrial [Ca(2+)]and [Na(+)], we previously showed that mitochondria buffer both subplasmalemmal cytosolic [Ca(2+)] and [Na(+)] in vascular smooth muscle cells. We have now directly measured sarcoplasmic reticulum [Ca(2+)] in aortic smooth muscle cells, revealing that mitochondrial Na(+)/Ca(2+) exchanger inhibition with CGP-37157 impairs sarcoplasmic reticulum Ca(2+) refilling during purinergic stimulation. By overexpressing hFis1 to remove mitochondria from the subplasmalemmal space, we show that the rate and extent of sarcoplasmic reticulum refilling is augmented by a subpopulation of peripheral mitochondria. In ATP-stimulated cells, hFis-1-mediated relocalization of mitochondria impaired the sarcoplasmic reticulum refilling process and reduced mitochondrial [Ca(2+)] elevations, despite increased cytosolic [Ca(2+)] elevations. Reversal of plasmalemmal Na(+)/Ca(2+) exchange was the primary Ca(2+) entry mechanism following ATP stimulation, based on the effects of KB-R7943. We propose that subplasmalemmal mitochondria ensure efficient sarcoplasmic reticulum refilling by cooperating with the plasmalemmal Na(+)/Ca(2+) exchanger to funnel Ca(2+) into the sarcoplasmic reticulum and minimize cytosolic [Ca(2+)] elevations that might otherwise contribute to hypertensive or proliferative vasculopathies.

Authors+Show Affiliations

Department of Cell Physiology and Metabolism, University of Geneva, 1 Michel-Servet, CH-1211 Geneva 4, Switzerland. Damon.Poburko@medecine.unige.chNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19023135

Citation

Poburko, Damon, et al. "Mitochondrial Regulation of Sarcoplasmic Reticulum Ca2+ Content in Vascular Smooth Muscle Cells." Circulation Research, vol. 104, no. 1, 2009, pp. 104-12.
Poburko D, Liao CH, van Breemen C, et al. Mitochondrial regulation of sarcoplasmic reticulum Ca2+ content in vascular smooth muscle cells. Circ Res. 2009;104(1):104-12.
Poburko, D., Liao, C. H., van Breemen, C., & Demaurex, N. (2009). Mitochondrial regulation of sarcoplasmic reticulum Ca2+ content in vascular smooth muscle cells. Circulation Research, 104(1), 104-12. https://doi.org/10.1161/CIRCRESAHA.108.180612
Poburko D, et al. Mitochondrial Regulation of Sarcoplasmic Reticulum Ca2+ Content in Vascular Smooth Muscle Cells. Circ Res. 2009 Jan 2;104(1):104-12. PubMed PMID: 19023135.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial regulation of sarcoplasmic reticulum Ca2+ content in vascular smooth muscle cells. AU - Poburko,Damon, AU - Liao,Chiu-Hsiang, AU - van Breemen,Cornelis, AU - Demaurex,Nicolas, Y1 - 2008/11/20/ PY - 2008/11/22/pubmed PY - 2009/2/12/medline PY - 2008/11/22/entrez SP - 104 EP - 12 JF - Circulation research JO - Circ Res VL - 104 IS - 1 N2 - Subplasmalemmal ion fluxes have global effects on Ca(2+) signaling in vascular smooth muscle. Measuring cytoplasmic and mitochondrial [Ca(2+)]and [Na(+)], we previously showed that mitochondria buffer both subplasmalemmal cytosolic [Ca(2+)] and [Na(+)] in vascular smooth muscle cells. We have now directly measured sarcoplasmic reticulum [Ca(2+)] in aortic smooth muscle cells, revealing that mitochondrial Na(+)/Ca(2+) exchanger inhibition with CGP-37157 impairs sarcoplasmic reticulum Ca(2+) refilling during purinergic stimulation. By overexpressing hFis1 to remove mitochondria from the subplasmalemmal space, we show that the rate and extent of sarcoplasmic reticulum refilling is augmented by a subpopulation of peripheral mitochondria. In ATP-stimulated cells, hFis-1-mediated relocalization of mitochondria impaired the sarcoplasmic reticulum refilling process and reduced mitochondrial [Ca(2+)] elevations, despite increased cytosolic [Ca(2+)] elevations. Reversal of plasmalemmal Na(+)/Ca(2+) exchange was the primary Ca(2+) entry mechanism following ATP stimulation, based on the effects of KB-R7943. We propose that subplasmalemmal mitochondria ensure efficient sarcoplasmic reticulum refilling by cooperating with the plasmalemmal Na(+)/Ca(2+) exchanger to funnel Ca(2+) into the sarcoplasmic reticulum and minimize cytosolic [Ca(2+)] elevations that might otherwise contribute to hypertensive or proliferative vasculopathies. SN - 1524-4571 UR - https://www.unboundmedicine.com/medline/citation/19023135/Mitochondrial_regulation_of_sarcoplasmic_reticulum_Ca2+_content_in_vascular_smooth_muscle_cells_ L2 - https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.108.180612?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -