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2-O-methyl PAF as a Ca2+ mobilizer in Madin Darby canine kidney cells

  • Jeng Hsien Yeh
  • , Chun Jen Huang
  • , Jang Hwa Lee
  • , Shu Shong Hsu
  • , Jin Shyr Chen
  • , He Hsiung Cheng
  • , Hong Tai Chang
  • , Jong Khing Huang
  • , Hsiao Min Chung
  • , Yeh Mei-Yin
  • , Chung Ren Jan*
  • *此作品的通信作者
  • Veterans General Hospital-Kaohsiung Taiwan
  • Chung Hwa University of Medical Technology
  • Tian-Sheng Memorial Hospital
  • Kaohsiung Medical University

研究成果: 期刊稿件 › 文章 › 同行評審

2 引文 斯高帕斯(Scopus)

摘要

In Madin-Darby canine kidney (MDCK) cells, the effect of 2-O-methyl PAF, an inactive analogue of platelet activating factor (PAF), on intracellular Ca 2+ concentration ([Ca2+]i) was measured by using the Ca2+-sensitive fluorescent dye fura-2. 2-O-methyl PAF (≥15 μM) caused a rapid rise of [Ca2+]i in a concentration-dependent manner. 2-O-methyl PAF-induced [Ca2+] i rise was partly reduced by removal of extracellular Ca 2+. 2-O-methyl PAF-induced extracellular Ca2+ influx was also suggested by Mn2+ influx-induced fura-2 fluorescence quench. The 2-O-methyl PAF-induced Ca2+ influx was blocked by nifedipine, verapamil and diltiazem. In Ca2+-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+-ATPase, caused a monophasic [Ca2+]i rise, after which 2-O-methyl PAF failed to increase [Ca2+]i; also, pretreatment with 2-O-methyl PAF depleted thapsigargin-sensitive Ca2+ stores. U73122, an inhibitor of phospholipase C, abolished ATP (but not 2-O-methyl PAF)-induced [Ca 2+]i rise. These findings suggest that 2-O-methyl PAF evokes a rapid increase in [Ca2+]i in renal tubular cells by stimulating both extracellular Ca2+ influx and intracellular Ca2+ release.

原文英語
頁(從 - 到)336-344
頁數9
期刊Life Sciences
卷77
發行號3
DOIs
出版狀態已出版 - 03 06 2005
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