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Blood, 1 July 2005, Vol. 106, No. 1, pp. 86-94.
Prepublished online as a Blood First Edition Paper on March 15, 2005; DOI 10.1182/blood-2004-09-3417.
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HEMATOPOIESIS
VCAM-1 expression in adult hematopoietic and nonhematopoietic cells is controlled by tissue-inductive signals and reflects their developmental origin
Tatiana Ulyanova,
Linda M. Scott,
Gregory V. Priestley,
Yi Jiang,
Betty Nakamoto,
Pandelakis A. Koni, and
Thalia Papayannopoulou
From the Division of Hematology, University of Washington, Seattle, WA; and the Program in Molecular Immunology, Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta.
Although expression of vascular cell adhesion molecule 1 (VCAM-1) in endothelial cells and its functional implications have been previously appreciated, VCAM-1 expression in other than endothelial cells, especially hematopoietic cells, has been recently recognized and has not been explored in detail. Using normal mice and mice with a conditional ablation of VCAM-1 through a Tie2-driven cre transgene, we have studied the biodistribution and the pattern of VCAM-1 expression in circulating versus tissue-residing cells before and after their enforced mobilization. In the normal mouse, both at basal hematopoiesis or following mobilization, VCAM-1 expression is confined to myeloid cells residing in hematopoietic tissues, whereas free cells in circulation or in body cavities are devoid of VCAM-1 messenger RNA (mRNA) and protein. However, following culture, proliferating myeloid cells, but not lymphoid cells, express VCAM-1. In the VCAM-1–ablated mouse, there is an increase in circulating progenitors as a consequence of their ongoing release from bone marrow, a process enhanced by splenectomy. We postulate that the main mechanism leading to their release is the ablation of VCAM-1 by fibroblastic and by endothelial cells. Ablation of VCAM-1 in fibroblasts by Tie2-driven cre is a novel finding and likely denotes their developmental ancestry by Tie2-expressing (mesenchymal?) progenitor cells during development.
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