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Retinoic acid suppresses endothelin-1 gene expression at the transcription level in endothelial cells

J Yokota1, M Kawana, C Hidai

  • 1Department of Cardiology, The Heart Institute of Japan, Tokyo Women's Medical University, 8-1 Kawadacho, Shinjuku-ku, 162-8666, Tokyo, Japan.

Atherosclerosis
|December 4, 2001
PubMed

Insights

Retinoids, including all-trans retinoic acid (ATRA), suppress endothelin-1 (ET-1) gene expression in endothelial cells. This suggests retinoids may modulate vascular function by regulating vasoactive substances at the transcriptional level.

Area of Science:

  • Vascular Biology
  • Molecular Endocrinology
  • Pharmacology

Background:

  • Retinoids inhibit cell growth, potentially offering anti-atherosclerotic effects.
  • Endothelin-1 (ET-1), a vasoconstrictor peptide, promotes vascular smooth muscle cell proliferation.

Purpose of the Study:

  • To investigate the impact of retinoids on endothelin-1 (ET-1) gene expression and transcriptional activity in endothelial cells.

Main Methods:

  • Cultured endothelial cells were treated with all-trans retinoic acid (ATRA), synthetic retinoids (Ch55, Am580), and an RAR antagonist (LE540).
  • ET-1 mRNA expression and half-life were analyzed.
  • Transfection experiments utilized a 5 kb ET-1 promoter-reporter gene construct to assess transcriptional activity.

Main Results:

  • ATRA suppressed ET-1 mRNA expression.
  • Synthetic retinoids (Ch55, Am580) significantly enhanced this suppression.
  • An RAR antagonist (LE540) blocked the inhibitory effect of retinoids on ET-1 gene expression.
  • ATRA did not alter ET-1 mRNA half-life.
  • ATRA and Ch55 reduced ET-1 promoter activity, indicating transcriptional down-regulation.

Conclusions:

  • Retinoids, acting through retinoic acid receptors (RARs), down-regulate ET-1 gene transcription in endothelial cells.
  • Retinoids represent potential modulators of endothelial cell function via transcriptional regulation of vasoactive substances.

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