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Related Experiment Videos

Ca2+-mediated ascorbate release from coronary artery endothelial cells.

Kim A Davis1, Sue E Samson, Kelly Best

  • 1Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

British Journal of Pharmacology
|December 7, 2005
PubMed
Summary
This summary is machine-generated.

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Calcium signaling in pig coronary artery endothelial cells (PCEC) triggers ascorbate release. ATP and calcium ionophores stimulate this release via P2Y2-like receptors, indicating a novel pathway for vitamin C regulation in these cells.

Area of Science:

  • Cardiovascular Biology
  • Cell Physiology
  • Biochemistry

Background:

  • Endothelial cells play a crucial role in vascular health.
  • Ascorbate (vitamin C) is a vital antioxidant with potential roles in endothelial function.
  • Mechanisms regulating ascorbate release from coronary artery endothelial cells are not fully understood.

Purpose of the Study:

  • To investigate the role of calcium ions (Ca2+) and ATP in regulating ascorbate release from pig coronary artery endothelial cells (PCEC).
  • To characterize the signaling pathways involved in ATP- and Ca2+-mediated ascorbate release.
  • To determine if PCEC possess a distinct Ca2+-mediated ascorbate release pathway.

Main Methods:

  • Primary culture of PCEC and pig coronary artery smooth muscle cells.

Related Experiment Videos

  • Stimulation with Ca2+ ionophore A23187, ATP, and ATP analogs.
  • Measurement of intracellular Ca2+ levels.
  • Inhibition studies using suramin and phospholipase C inhibitor U73122.
  • Ascorbate uptake assays at varying concentrations.

    • Main Results:

    • ATP and Ca2+ ionophore A23187 significantly potentiated ascorbate release from PCEC.
    • ATP-induced release was mediated by P2Y2-like receptors and was dependent on extracellular and intracellular Ca2+.
    • Ascorbate uptake was differentially affected by ATP and A23187 depending on the extracellular ascorbate concentration.
    • A Ca2+-mediated ascorbate release pathway was identified in PCEC but not in smooth muscle cells.

    Conclusions:

    • PCEC possess a Ca2+-dependent pathway for releasing ascorbate, which can be activated by extracellular ATP.
    • This pathway involves P2Y2-like receptors and intracellular Ca2+ mobilization.
    • The findings reveal a novel mechanism for regulating ascorbate levels in the coronary vasculature.