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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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Submitted July 13, 2007
Accepted January 16, 2008

Erythroid defects in TR{alpha}-/- mice

Tulene S. Kendrick, Christine J. Payne, Michael R. Epis, Jessica R. Schneider, Peter J. Leedman, S. Peter Klinken*, and Evan Ingley

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

* Corresponding author; email: pklinken{at}waimr.uwa.edu.au.

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 hematrocrits, 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, demonstrating the importance of TR{alpha} to the erythroid compartment.


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