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 Blood, 1 June 2004, Vol. 103, No. 11, pp. 4084-4092.
Prepublished online as a Blood First Edition Paper on February 12, 2004; DOI 10.1182/blood-2003-06-1827.

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HEMATOPOIESIS

The role of apoptosis in the development of AGM hematopoietic stem cells revealed by Bcl-2 overexpression

Claudia Orelio, Kirsty N. Harvey, Colin Miles, Robert A. J. Oostendorp, Karin van der Horn, and Elaine Dzierzak

From the Department of Cell Biology and Genetics, Erasmus University Medical Centre, Rotterdam, The Netherlands; Institute of Human Genetics, International Centre for Life, Newcastle-upon-Tyne, United Kingdom; and Labor für Stammzellphysiologie, III Medizinische Klinik und Poliklinik, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany.

Apoptosis is an essential process in embryonic tissue remodeling and adult tissue homeostasis. Within the adult hematopoietic system, it allows for tight regulation of hematopoietic cell subsets. Previously, it was shown that B-cell leukemia 2 (Bcl-2) overexpression in the adult increases the viability and activity of hematopoietic cells under normal and/or stressful conditions. However, a role for apoptosis in the embryonic hematopoietic system has not yet been established. Since the first hematopoietic stem cells (HSCs) are generated within the aortagonad-mesonephros (AGM; an actively remodeling tissue) region beginning at embryonic day 10.5, we examined this tissue for expression of apoptosis-related genes and ongoing apoptosis. Here, we show expression of several proapoptotic and antiapoptotic genes in the AGM. We also generated transgenic mice overexpressing Bcl-2 under the control of the transcriptional regulatory elements of the HSC marker stem cell antigen-1 (Sca-1), to test for the role of cell survival in the regulation of AGM HSCs. We provide evidence for increased numbers and viability of Sca-1+ cells in the AGM and subdissected midgestation aortas, the site where HSCs are localized. Most important, our in vivo transplantation data show that Bcl-2 overexpression increases AGM and fetal liver HSC activity, strongly suggesting that apoptosis plays a role in HSC development.


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