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Thyroid hormone induces erythropoietin gene expression through augmented accumulation of hypoxia-inducible factor-1
Erythropoietin (Epo) and thyroid hormone (T(3)) are key molecules in the development of red blood cells.
Effects of thyroid hormones on the production of erythropoietin (Epo) were investigated in isolated perfused rat kidneys and in the human hepatoma cell line, HepG2. Epo protein was measured by radioimmunoassay. L-triiodothyronine and L-thyroxine stimulated hypoxia-induced Epo formation both in the kidney and in HepG2 cells in a dose-dependent fashion. Quantitation of Epo mRNA by competitive polymerase chain reaction (PCR) showed that hypoxic HepG2 cells had three-fold higher Epo messenger RNA levels when treated with thyroid hormones for 3 hours. Measurements of oxygen consumption revealed that this effect was not due to an increase in the degree of hypoxia. Thus, apart from the known direct effect on erythroid precursors, thyroid hormones appear to stimulate erythropoiesis by a noncalorigenic increase in Epo production
Institute of Physiology I, University of Bonn, Germany.
Laboratory experiments have demonstrated that tetra- and triiodothyronine (T4, T3) enhance hypoxia-induced erythropoietin (Epo) production.
EPO secretion is regulated endocrinologically. Thyroid hormones and adrenocortical hormone enhance EPO secretion (Peschle et al. 1978, Nagy & Berczi 1989, Brenner et al. 1994, Fandrey et al. 1994).
Wolff M & Jelkmann W 1994 Thyroid hormones enhance hypoxia-induced erythropoietin production in vitro. Experimental Hematology 22 272–277.
Area: Biochemistry
Posted By: Kelleen Flaherty, Staff, Biology/Invertebrate Zoology
"However these and any other stimuli for release of EPO will only be
secondary. Certain androgens can also have a secondary effect on EPO, as can thyroxine,
a metabolic hormone produce by the thyroid gland."