P2X<sub>4</sub> receptors mediate ATP-induced calcium influx in human vascular endothelial cells

DOI Web Site PubMed 被引用文献17件
  • Zhi Qi
    Department of Physiology, Nagoya University School of Medicine, Nagoya 464-8601, Japan
  • Masahiro Sokabe
    Department of Physiology, Nagoya University School of Medicine, Nagoya 464-8601, Japan
  • Joji Ando
    Department of Biomedical Engineering, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033; and
  • Akira Kamiya
    Department of Biomedical Engineering, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033; and
  • Kimiko Yamamoto
    Department of Biomedical Engineering, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033; and
  • Risa Korenaga
    Department of Biomedical Engineering, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033; and

書誌事項

公開日
2000-07-01
DOI
  • 10.1152/ajpheart.2000.279.1.h285
公開者
American Physiological Society

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説明

<jats:p> ATP induces Ca<jats:sup>2+</jats:sup> influx across the cell membrane and activates release from intracellular Ca<jats:sup>2+</jats:sup> pools in vascular endothelial cells (ECs). Ca<jats:sup>2+</jats:sup> signaling leads to the modification of a variety of EC functions, including the production of vasoactive substances such as nitric oxide and prostacyclin. However, the molecular mechanisms for ATP-induced Ca<jats:sup>2+</jats:sup> influx in ECs have not been thoroughly clarified. Here we demonstrate evidence that a P2X<jats:sub>4</jats:sub>receptor for an ATP-gated cation channel is predominantly expressed in human ECs and is involved in the ATP-induced Ca<jats:sup>2+</jats:sup> influx. Northern blot analysis distinctly showed the expression of P2X<jats:sub>4</jats:sub> mRNA in human ECs cultured from the umbilical vein, aorta, pulmonary artery, and skin microvessels. Competitive PCR revealed that P2X<jats:sub>4</jats:sub> mRNA expression was much higher in ECs than was the expression of other subtypes, including P2X<jats:sub>1</jats:sub>, P2X<jats:sub>3</jats:sub>, P2X<jats:sub>5</jats:sub>, and P2X<jats:sub>7</jats:sub>. Treatment of ECs with antisense oligonucleotides designed to target the P2X<jats:sub>4</jats:sub> receptor decreased the P2X<jats:sub>4</jats:sub> mRNA and protein levels to ∼25% of control levels and markedly prevented the ATP-induced Ca<jats:sup>2+</jats:sup> influx. </jats:p>

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