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Thyroid hormone inhibits vascular remodeling through suppression of cAMP response element binding protein activity

Kae Fukuyama1, Toshihiro Ichiki, Ikuyo Imayama

  • 1Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku, 812-8582 Fukuoka, Japan.

Arteriosclerosis, Thrombosis, and Vascular Biology
|June 24, 2006
PubMed

Insights

Thyroid hormone (T3) inhibits the angiotensin II-induced activation of CREB signaling, reducing vascular smooth muscle cell proliferation and cytokine expression, thereby offering an anti-atherosclerotic effect.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Molecular Biology

Background:

  • Impaired thyroid function is linked to ischemic heart disease.
  • The molecular mechanisms behind thyroid hormone's anti-atherosclerotic effects are not well understood.
  • Angiotensin II (Ang II) plays a key role in cardiovascular disease.

Purpose of the Study:

  • To investigate if thyroid hormone influences the Ang II signaling pathway.
  • To elucidate the molecular mechanisms of thyroid hormone's anti-atherosclerotic actions.

Main Methods:

  • Examined the effect of 3,3',5-triiodo-L-thyronine (T3) on Ang II-induced signaling in vascular smooth muscle cells (VSMCs).
  • Assessed the interaction between thyroid hormone receptor and cAMP response element (CRE) binding protein (CREB).
  • Evaluated T3's impact on interleukin-6 (IL-6) mRNA expression and CRE-dependent promoter activity.
  • Administered T3 to rats undergoing balloon injury to assess neointimal formation.

Main Results:

  • T3 did not affect Ang II-induced ERK or p38 MAPK activation in VSMCs.
  • T3 inhibited Ang II-induced CREB activation and protein-protein interaction between thyroid hormone receptor and CREB.
  • T3 reduced Ang II-induced IL-6 mRNA expression, CRE-dependent promoter activity, and protein synthesis.
  • T3 administration in rats attenuated neointimal formation, with decreased CREB activation and BrdU incorporation.

Conclusions:

  • T3 inhibits the CREB/CRE signaling pathway.
  • T3 suppresses cytokine expression and VSMC proliferation.
  • These actions may contribute to the anti-atherosclerotic effects of thyroid hormone.
Abstract

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