Endothelin induces transcription of fos/jun family genes: A prominent role for calcium ion

David Pribnow, Leslie L. Muldoon, Mark Fajardo, Livia Theodor, Li Ye Stephen Chen, Bruce E. Magun

Research output: Contribution to journalArticle

55 Scopus citations

Abstract

The 21-amino acid mammalian peptide endothelin (ET) is a powerful vasoconstrictor, a mitogen for fibroblasts and vascular smooth muscle cells, and a potent effector for numerous tissues. Through extracellular interaction with G protein-coupled transmembrane receptors, ET stimulates intracellular second messenger events that in turn activate immediate early gene transcription. Using Northern blot hybridization and nuclear run-on analyses, we examined the modulation of c-fos, fos-B, fra-1, c-jun, and jun-B gene transcripts in Rat-1 fibroblasts after ET treatment. Furthermore, we investigated the role that intracellular Ca2+ transients played in effecting this gene regulation, using the intracellular Ca2+ chelator 1, 2-bis(o-aminophenoxy)ethane-N, N, N’, N’-tetraacetic acid (BAPTA) to block Ca2+-dependent transcription. Our results demonstrate that ET rapidly effects increased RNA levels for all five fos/jun family genes investigated, at least two of them by increasing gene transcription. Furthermore, our results argue that increased intracellular free Ca2+ is directly involved in the induction of these fos/jun family genes by ET. While mobilization of intracellular Ca2+ is not the only pathway to fos/jun gene induction used by ET, it is clearly a major component of the signaling apparatus that is set in motion by this potent effector.

Original languageEnglish (US)
Pages (from-to)1003-1012
Number of pages10
JournalMolecular Endocrinology
Volume6
Issue number7
DOIs
StatePublished - Jul 1 1992

ASJC Scopus subject areas

  • Molecular Biology
  • Endocrinology

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