Thyroid hormone and its cognate receptor (TR) have been implicated in the production of red blood cells. Here, we show mice deficient for TR␣ have compromised fetal and adult erythropoiesis. Erythroid progenitor numbers were significantly reduced in TR␣ Ϫ/Ϫ fetal livers, and transit through the final stages of maturation was impeded. In addition, immortalized TR␣ Ϫ/Ϫ erythroblasts displayed increased apoptosis and reduced capacity for proliferation and differentiation. Adult TR␣ Ϫ/Ϫ mice had lower hematocrit levels, elevated glucocorticoid levels, and an altered stress erythropoiesis response to hemolytic anemia. Most TR␣ Ϫ/Ϫ animals contained markedly altered progenitor numbers in their spleens. Strikingly, 20% of TR␣ Ϫ/Ϫ 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␣ Ϫ/Ϫ mice, demonstrating the importance of TR␣ to the erythroid compartment. (Blood. 2008;111: 3245-3248)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.