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Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells.

Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells. Research Abstract Details 

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  • Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells. Abstract Text:

    h joussetH Jousset,r malliR Malli,n girardinN Girardin,w f graierW F Graier,n demaurexN Demaurex,m friedenM Frieden,

    Ca(2+) entry in endothelial cells is a key signaling event as it prolongs the Ca(2+) signal activated by a receptor agonist, and thus allows an adequate production of a variety of compounds. The possible routes that lead to Ca(2+) entry in non-excitable cells include the receptor-activated Ca(2+) entry (RACE), which requires the presence of an agonist to be activated, and the store-operated Ca(2+) entry (SOCE) pathway, whose activation requires the depletion of the ER Ca(2+) store. However, the relative importance of these two influx pathways during physiological stimulation is not known. In the present study we experimentally differentiated these two types of influxes and determined under which circumstances they are activated. We show that La(3+) (at 10muM) is a discriminating compound that efficiently blocks SOCE but is almost without effect on histamine-induced Ca(2+) entry (RACE). In line with this, histamine does not induce massive store depletion when performed in the presence of extracellular Ca(2+). In addition, inhibition of mitochondrial respiration significantly reduces SOCE but modestly affects RACE. Thus, agonist-induced Ca(2+) entry is insensitive to La(3+), and only modestly affected by mitochondrial depolarization. These data shows that agonist relies almost exclusively on RACE for sustained Ca(2+) signaling in endothelial cells.

    Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells. Publishing Authors By Initials

    h joussetH Jousset,r malliR Malli,n girardinN Girardin,wf graierWF Graier,n demaurexN Demaurex,m friedenM Frieden,

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    Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Cell calcium

    VOLUME: 43

    Page Numbers: 83-94

    Journal Abbreviation: Cell Calcium

    ISSN: 0143-4160

    DAY: 4

    MONTH: 06

    YEAR: 2007

    Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells. Information

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    LANGUAGE: eng

    NlmUniqueID: 8006226

    Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells. Keywords Mesh Terms:

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    Grant and Affiliation Information for Evidence for a receptor-activated Ca(2+) entry pathway independent from Ca(2+) store depletion in endothelial cells.

    AFFILIATION: Department of Cell Physiology and Metabolism, Geneva Medical Center, 1 rue Michel Servet, 1211 Geneva 4, Switzerland.

    Country: Scotland

    Scotland Research PublicationScotland Research Publication

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    MEDLINETA: Cell Calcium

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