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 Blood, 5 November 2009, Vol. 114, No. 19, pp. 4045-4053.
Prepublished online as a Blood First Edition Paper on September 4, 2009; DOI 10.1182/blood-2008-08-169474.

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HEMATOPOIESIS AND STEM CELLS

Erythroid dysplasia, megaloblastic anemia, and impaired lymphopoiesis arising from mitochondrial dysfunction

Michael L. Chen1, T. Daniel Logan1, Maryann L. Hochberg2, Suresh G. Shelat3, Xiang Yu4, Gregory E. Wilding5,6, Wei Tan6, Gregory C. Kujoth7, Tomas A. Prolla7, Mary A. Selak8, Mondira Kundu9, Martin Carroll1, and James E. Thompson1,2

1 Division of Hematology and Oncology, Department of Medicine, University of Pennsylvania, Philadelphia; 2 Departments of Medicine and Immunology, Roswell Park Cancer Institute, Buffalo, NY; 3 Department of Pathology and Laboratory Medicine and 4 Cell and Molecular Biology Graduate Group, University of Pennsylvania, Philadelphia; 5 Department of Biostatistics, The State University of New York at Buffalo; 6 Department of Biostatistics, Roswell Park Cancer Institute, Buffalo, NY; 7 Departments of Genetics and Medical Genetics, University of Wisconsin, Madison; 8 Children's Hospital of Philadelphia Research Institute, Children's Hospital of Philadelphia and University of Pennsylvania; and 9 Department of Pathology, St Jude Children's Research Hospital, Memphis, TN

Recent reports describe hematopoietic abnormalities in mice with targeted instability of the mitochondrial genome. However, these abnormalities have not been fully described. We demonstrate that mutant animals develop an age-dependent, macrocytic anemia with abnormal erythroid maturation and megaloblastic changes, as well as profound defects in lymphopoiesis. Mice die of severe fatal anemia at 15 months of age. Bone-marrow transplantation studies demonstrate that these abnormalities are intrinsic to the hematopoietic compartment and dependent upon the age of donor hematopoietic stem cells. These abnormalities are phenotypically similar to those found in patients with refractory anemia, suggesting that, in some cases, the myelodysplastic syndromes are caused by abnormalities of mitochondrial function.


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