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Blood, 1 May 2004, Vol. 103, No. 9, pp. 3258-3264.
Prepublished online as a Blood First Edition Paper on January 15, 2004; DOI 10.1182/blood-2003-11-4011.
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PLENARY PAPERS
Hematopoiesis is severely altered in mice with an induced osteoblast deficiency
Dora Visnjic,
Zana Kalajzic,
David W. Rowe,
Vedran Katavic,
Joseph Lorenzo, and
Hector L. Aguila
From the Department of Genetics and Developmental Biology; Division of Endocrinology, Department of Medicine; and Center for Immunotherapy of Cancer and Infectious Diseases, Department of Medicine, University of Connecticut Health Center, Farmington.
We previously reported a transgenic mouse model expressing herpesvirus thymidine kinase (TK) gene under the control of a 2.3-kilobase fragment of the rat collagen  1 type I promoter (Col2.3 TK). This construct confers lineage-specific expression in developing osteoblasts, allowing the conditional ablation of osteoblast lineage after treatment with ganciclovir (GCV). After GCV treatment these mice have profound alterations on bone formation leading to a progressive bone loss. In addition, treated animals also lose bone marrow cellularity. In this report we characterized hematopoietic parameters in GCV-treated Col2.3TK mice, and we show that after treatment transgenic animals lose lymphoid, erythroid, and myeloid progenitors in the bone marrow, followed by decreases in the number of hematopoietic stem cells (HSCs). Together with the decrease in bone marrow hematopoiesis, active extramedullary hematopoiesis was observed in the spleen and liver, as measured by an increase in peripheral HSCs and active primary in vitro hematopoiesis. After withdrawal of GCV, osteoblasts reappeared in the bone compartment together with a recovery of medullary and decrease in extramedullary hematopoiesis. These observations directly demonstrate the role of osteoblasts in hematopoiesis and provide a model to study the interactions between the mesenchymal and hematopoietic compartments in the marrow. (Blood. 2004; 103:3258-3264)
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