Thyroid hormone and angiogenesis

Mary K. Luidens, Shaker A. Mousa, Faith B. Davis, Hung Y. Lin, Paul J. Davis

Research output: Contribution to journalReview article

73 Citations (Scopus)

Abstract

In models of thyroid hormone-induced cardiac hypertrophy, there is appropriate, supportive angiogenesis. Twenty years ago in one such model, angiogenesis in response to the hormone was observed before hypertrophy developed and it is now understood that iodothyronines induce neovascularization in a variety of settings, including the heart, ischemic striated muscle and tumor beds. The molecular mechanism of the proangiogenic action of thyroid hormone is both nongenomic and genomic. It is initiated nongenomically at the cell surface receptor for the hormone on integrin αvβ3. Kinase transduction of the hormone signal and, ultimately, transcription of several anagiogenesis-relevant genes result. The genes include basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF). In addition, the integrin receptor for thyroid hormone (l-thyroxine, T4, and 3, 5, 3′-triiodo-l-thyronine, T3) engages in crosstalk with the VEGF and bFGF receptors. Occlusion with tetraiodothyroacetic acid (tetrac) of the hormone receptor on the integrin in the absence of T4 and T3 suppresses the angiogenic effects of VEGF and bFGF. Tetrac also blocks the proangiogenic actions of T4 and T3. Other thyroid hormone analogues that are angiogenic include diiodothyropropionic acid (DITPA) and the nuclear thyroid hormone receptor-β-selective agonist, GC-1. Thyroid hormone sustains angiogenesis and coronary blood flow about infarcted heart tissue in experimental models and blocks deleterious heart remodeling that otherwise is predictable in such tissue. The hormone may also induce expression of the hypoxia-inducible factor 1α (HIF1α) gene, a transcription factor important to coronary artery collateralization in the setting of hypoxia. The hormone also causes transcription of the matrix Gla protein (MGP) gene that opposes vascular smooth muscle calcification.

Original languageEnglish
Pages (from-to)142-145
Number of pages4
JournalVascular Pharmacology
Volume52
Issue number3-4
DOIs
Publication statusPublished - Mar 2010
Externally publishedYes

Fingerprint

Thyroid Hormones
Hormones
Fibroblast Growth Factor 2
Integrins
Vascular Endothelial Growth Factor A
Thyroid Hormone Receptors
Genes
Thyronines
Hypoxia-Inducible Factor 1
Fibroblast Growth Factor Receptors
Heart Block
Striated Muscle
Cardiomegaly
Cell Surface Receptors
Cytoplasmic and Nuclear Receptors
Thyroxine
Vascular Smooth Muscle
Hypertrophy
Signal Transduction
Coronary Vessels

Keywords

  • 3 5, 3′-triiodothyronine
  • Integrin αvβ3
  • l-thyroxine
  • Nongenomic actions
  • Tetraiodothyroacetic acid

ASJC Scopus subject areas

  • Molecular Medicine
  • Physiology
  • Pharmacology

Cite this

Luidens, M. K., Mousa, S. A., Davis, F. B., Lin, H. Y., & Davis, P. J. (2010). Thyroid hormone and angiogenesis. Vascular Pharmacology, 52(3-4), 142-145. https://doi.org/10.1016/j.vph.2009.10.007

Thyroid hormone and angiogenesis. / Luidens, Mary K.; Mousa, Shaker A.; Davis, Faith B.; Lin, Hung Y.; Davis, Paul J.

In: Vascular Pharmacology, Vol. 52, No. 3-4, 03.2010, p. 142-145.

Research output: Contribution to journalReview article

Luidens, MK, Mousa, SA, Davis, FB, Lin, HY & Davis, PJ 2010, 'Thyroid hormone and angiogenesis', Vascular Pharmacology, vol. 52, no. 3-4, pp. 142-145. https://doi.org/10.1016/j.vph.2009.10.007
Luidens MK, Mousa SA, Davis FB, Lin HY, Davis PJ. Thyroid hormone and angiogenesis. Vascular Pharmacology. 2010 Mar;52(3-4):142-145. https://doi.org/10.1016/j.vph.2009.10.007
Luidens, Mary K. ; Mousa, Shaker A. ; Davis, Faith B. ; Lin, Hung Y. ; Davis, Paul J. / Thyroid hormone and angiogenesis. In: Vascular Pharmacology. 2010 ; Vol. 52, No. 3-4. pp. 142-145.
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