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Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
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Modified In Vivo Matrix Gel Plug Assay for Angiogenesis Studies
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Published on: June 30, 2023

Thyroid hormone and angiogenesis.

Mary K Luidens1, Shaker A Mousa, Faith B Davis

  • 1Signal Transduction Laboratory, Ordway Research Institute, Albany, NY 12208, USA.

Vascular Pharmacology
|November 3, 2009
PubMed
Summary
This summary is machine-generated.

Thyroid hormone promotes blood vessel growth (angiogenesis) through both cell surface and genomic pathways. This process supports heart health, particularly after injury, and influences blood vessel development in various tissues.

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Area of Science:

  • Cardiovascular Research
  • Endocrinology
  • Molecular Biology

Background:

  • Thyroid hormone is known to induce cardiac hypertrophy.
  • Angiogenesis, or new blood vessel formation, is crucial for tissue health and repair.
  • The precise molecular mechanisms of thyroid hormone's proangiogenic effects were not fully elucidated.

Purpose of the Study:

  • To investigate the molecular mechanisms by which thyroid hormone promotes angiogenesis.
  • To explore the role of thyroid hormone in supporting cardiovascular function and preventing adverse remodeling.

Main Methods:

  • Investigated thyroid hormone's action via cell surface integrin alphavbeta3 and genomic pathways.
  • Utilized specific inhibitors like tetraiodothyroacetic acid (tetrac) to block hormone receptor activity.
  • Examined the expression of key angiogenic genes such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF).

Main Results:

  • Thyroid hormone initiates proangiogenic signaling through integrin alphavbeta3, leading to gene transcription (VEGF, bFGF).
  • Thyroid hormone receptor interacts with VEGF and bFGF receptors, modulating their activity.
  • Inhibition of the integrin receptor blocks thyroid hormone's proangiogenic effects and gene expression.
  • Thyroid hormone analogs (DITPA, GC-1) also exhibit angiogenic properties.
  • Thyroid hormone supports angiogenesis in infarcted heart tissue, preventing detrimental remodeling and potentially influencing hypoxia-inducible factor 1alpha (HIF1alpha) and matrix Gla protein (MGP) gene expression.

Conclusions:

  • Thyroid hormone exerts proangiogenic effects through a dual nongenomic and genomic mechanism initiated at the cell surface.
  • This action is vital for supporting vascularization in the heart and other tissues, offering therapeutic potential.
  • Thyroid hormone's role extends to preventing adverse cardiac remodeling and influencing vascular calcification pathways.