Abstract
A series of reports in the past decade have ascribed pro-angiogenic activity to several thyroid hormone analogues, including L-thyroxine (T4), 3,5,3-triiodo-L-thyronine (T3) and diiodothyropropionic acid (DITPA). Model systems of angiogenesis have demonstrated that thyroid hormone-induced neovascularization is initiated at a cell surface receptor for the hormone on an integrin. The hormone signal is transduced within the cell by extracellular regulated kinase 1/2 (ERK1/2) into secretion of basic fibroblast growth factor (bFGF) and other vascular growth factors and consequent angiogenesis. Intact animal studies have shown that endogenous thyroid hormone supports blood vessel density in heart and brain and that thyroid hormone administration can induce angiogenesis in ischemic limbs.
Highlights
In studies of thyroid hormone-induced myocardial hypertrophy a decade ago, Tomanek and co-workers showed that administration of L-thyroxine (T4) to rats caused left ventricular capillary growth [1]
The epidermal growth factor (EGF)-like ligands bind to the cell surface EGF receptor (EGFR) and may have their signals amplified by action of thyroid hormone on the
If thyroid hormone receptor (TR) isoforms are involved in the pro-angiogenic action of iodothyronines that begin at the cell surface, this is an example of the interface of membrane-initiated actions and downstream effects involving TR in which thyroid hormone need not be present in the cell nucleus
Summary
In studies of thyroid hormone-induced myocardial hypertrophy a decade ago, Tomanek and co-workers showed that administration of L-thyroxine (T4) to rats caused left ventricular capillary growth [1]. A nuclear thyroid hormone receptor (TR) isoform [15] is not primarily involved in the pro-angiogenic action of the hormone. THYROID HORMONE ACTION AT ITS CELL SURFACE RECEPTOR ON INTEGRIN V3
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