Journal article
Erythroid defects in TR -/- mice
Blood, Vol.111(6), pp.3245-3248
2008
Abstract
Thyroid hormone and its cognate receptor (TR) have been implicated in the production of red blood cells. Here, we show mice deficient for TRα have compromised fetal and adult erythropoiesis. Erythroid progenitor numbers were significantly reduced in TRα -/- fetal livers, and transit through the final stages of maturation was impeded. In addition, immortalized TRα -/- erythroblasts displayed increased apoptosis and reduced capacity for proliferation and differentiation. Adult TRα -/- mice had lower hematocrit levels, elevated glucocorticoid levels, and an altered stress erythropoiesis response to hemolytic anemia. Most TRα -/- animals contained markedly altered progenitor numbers in their spleens. Strikingly, 20% of TRα -/- mice failed to elicit a stress erythropoiesis response and recovered very poorly from hemolytic anemia. We conclude that an underlying erythroid defect exists in TRα -/- mice, demonstrating the importance of TRα to the erythroid compartment.
Details
- Title
- Erythroid defects in TR -/- mice
- Authors/Creators
- T.S. Kendrick (Author/Creator)C.J. Payne (Author/Creator)M.R. Epis (Author/Creator)J.R. Schneider (Author/Creator)P.J. Leedman (Author/Creator)S.P. Klinken (Author/Creator)E. Ingley (Author/Creator)
- Publication Details
- Blood, Vol.111(6), pp.3245-3248
- Publisher
- American Society of Hematology
- Identifiers
- 991005545208107891
- Copyright
- © 2008 by The American Society of Hematology.
- Murdoch Affiliation
- Murdoch University
- Language
- English
- Resource Type
- Journal article
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- Collaboration types
- Domestic collaboration
- Citation topics
- 1 Clinical & Life Sciences
- 1.213 Thyroid Disorders
- 1.213.168 Thyroid Disorders
- Web Of Science research areas
- Hematology
- ESI research areas
- Clinical Medicine