Eicosapentaenoic acid triggers Ca2+ release and Ca2+ influx in mouse cerebral cortex endothelial bEND.3 cells

King Chuen Wu, Kar Lok Wong, Mei Ling Wang, Lian Ru Shiao, Iat Lon Leong, Chi Li Gong, Ka Shun Cheng, Paul Chan, Yuk Man Leung

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Eicosapentaenoic acid (EPA), an omega-3 fatty acid abundant in fish oil, protects endothelial cells (EC) from lipotoxicity and triggers EC NO release. The latter is related to an elevation of cytosolic Ca2+. Although EPA has been shown to cause human EC cytosolic Ca2+ elevation, the mechanism is unclear. Microfluorimetric imaging was used here to measure free cytosolic Ca2+ concentration. EPA was shown to cause intracellular Ca2+ release in mouse cerebral cortex endothelial bEND.3 cells; interestingly, the EPA-sensitive intracellular Ca2+ pool(s) appeared to encompass and was larger than the Ca2+ pool mobilized by sarcoplasmic-endoplasmic reticulum Ca2+-ATPase inhibition by cyclopiazonic acid. EPA also opened a Ca2+ influx pathway pharmacologically distinct from store-operated Ca2+ influx. Surprisingly, EPA-triggered Ca2+ influx was Ni2+-insensitive; and EPA did not trigger Mn2+ influx. Further, EPA-triggered Ca2+ influx did not involve Na+–Ca2+ exchangers. Thus, our results suggest EPA triggered unusual mechanisms of Ca2+ release and Ca2+ influx in EC.

Original languageEnglish
Pages (from-to)33-41
Number of pages9
JournalJournal of Physiological Sciences
Issue number1
Publication statusPublished - Jan 1 2018


  • Ca influx
  • Ca release
  • Eicosapentaenoic acid
  • Endothelial cells

ASJC Scopus subject areas

  • General Medicine


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