Depletion of [Ca2+](i) inhibits hypoxia-induced vascular permeability factor (vascular endothelial growth factor) gene expression

Debabrata Mukhopadhyay, Hamid I. Akbarali

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

We have investigated the role of ion channels and intracellular Ca2+ in the regulation of hypoxia-mediated VPF/VEGF activation. Known channel activator and blockers like lemakalim, glibenclamide, tetraethylammonium, 4-aminopyridine and nifedipine do not inhibit VPF/VEGF induction due to hypoxia. Whereas, 5 mM caffeine pretreatment of the 293 cells exhibits a complete inhibition of hypoxia inducted VPF/VEGF expression. Moreover, the cells treated with BAPTA-AM prior to hypoxia also show a dramatic decrease in the VPF/VEGF message level, which suggests an important role of intracellular Ca2+ in this signaling pathway. Caffeine pretreatment also inhibits hypoxia-mediated c-Src kinase activity. These findings demonstrate the importance of intracellular Ca2+ in the event of hypoxia-induced VPF/VEGF expression.

Original languageEnglish (US)
Pages (from-to)733-738
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume229
Issue number3
DOIs
StatePublished - Dec 24 1996

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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