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 Blood, 15 March 2008, Vol. 111, No. 6, pp. 3245-3248.
Prepublished online as a Blood First Edition Paper on January 18, 2008; DOI 10.1182/blood-2007-07-101105.

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RED CELLS

Brief Report

Erythroid defects in TR{alpha}–/– mice

Tulene S. Kendrick1,2, Christine J. Payne13, Michael R. Epis1, Jessica R. Schneider1,2, Peter J. Leedman1,3, S. Peter Klinken1, and Evan Ingley1,2

1 Laboratory for Cancer Medicine and 2 Cell Signalling Group, Western Australian Institute for Medical Research and Centre for Medical Research, The University of Western Australia, Perth; and 3 Royal Perth Hospital, Perth, Australia

Thyroid hormone and its cognate receptor (TR) have been implicated in the production of red blood cells. Here, we show mice deficient for TR{alpha} have compromised fetal and adult erythropoiesis. Erythroid progenitor numbers were significantly reduced in TR{alpha}–/– fetal livers, and transit through the final stages of maturation was impeded. In addition, immortalized TR{alpha}–/– erythroblasts displayed increased apoptosis and reduced capacity for proliferation and differentiation. Adult TR{alpha}–/– mice had lower hematocrit levels, elevated glucocorticoid levels, and an altered stress erythropoiesis response to hemolytic anemia. Most TR{alpha}–/– animals contained markedly altered progenitor numbers in their spleens. Strikingly, 20% of TR{alpha}–/– mice failed to elicit a stress erythropoiesis response and recovered very poorly from hemolytic anemia. We conclude that an underlying erythroid defect exists in TR{alpha}–/– mice, demon-strating the importance of TR{alpha} to the erythroid compartment.


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