Levels of normal or pathologic angiogenic activity are usually considered to be products of contributions from principal vascular growth factors and their specific receptors, of anatomic locations in specific organs or, particularly in cancer, of tissue oxygen tension and of pharmaceutical modulation. In this chapter, we examine the contributions of endocrine hormones-small molecules (steroids) and peptides-to regulation of angiogenesis. Most of the hormones considered appear to have actions on blood vessels only in specific tissues, but the angiogenic properties of these substances have not been systematically studied in tissues other than those that are classical targets. Estrogens and androgens have angiogenic actions, some of which are obtained exclusively in cells obtained, respectively, from female and male sources. Estrogen and progesterone contribute to uterine angiogenesis in the menstrual cycle. Glucocorticoids that lack classical glucocorticoid activities have been designed pharmaceutically to be angiostatic drugs. Among the peptide hormones, prolactin is angiogenic in certain tissues, but the hormone is proteolytically cleaved to yield angiostatic peptides. ACTH of course affects angiogenesis in the adrenal cortex, but the ACTH receptor may be expressed in other tissues, e.g., the placenta, which then may be the focus of ACTH-dependent angiogenesis. TSH is pro-angiogenic in the thyroid gland and supports tumor-related carcinoma of the thyroid, but the TSH receptor may be expressed in other tissues and, in such settings, circulating levels of TSH may be supporting new blood vessel formation. In a separate chapter we have described the angiogenic spectrum of thyroid hormone and its analogues.
|Title of host publication||Angiogenesis Modulations in Health and Disease: Practical Applications of Pro- and Anti-angiogenesis Targets|
|Number of pages||7|
|ISBN (Print)||9789400764675, 9400764669, 9789400764668|
|Publication status||Published - Nov 1 2013|
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