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Blood, 1 February 2006, Vol. 107, No. 3, pp. 1207-1213. Prepublished online as a Blood First Edition Paper on October 11, 2005; DOI 10.1182/blood-2005-05-1823. This Article Full Text (PDF) All Versions of this Article: 2005-05-1823v1 107/3/1207    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hamaguchi, I. Articles by Suda, T. Search for Related Content PubMed PubMed Citation Articles by Hamaguchi, I. Articles by Suda, T. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted May 5, 2005 Accepted September 27, 2005 Loss of Tie2 receptor compromises embryonic stem cell-derived endothelial but not hematopoietic cell survival Isao Hamaguchi*, Tohru Morisada, Masaki Azuma, Kyoko Murakami, Madoka Kuramitsu, Takuro Mizukami, Kazuyuki Ohbo, Kazunari Yamaguchi, Yuichi Oike, Daniel J Dumont, and Toshio Suda Department of Cell Differentiation, The Sakaguchi Laboratory, School of Medicine, Keio University, Tokyo, Japan; Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan Department of Cell Differentiation, The Sakaguchi Laboratory, School of Medicine, Keio University, Tokyo, Japan Department of Safety Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan Department of Medical Biophysics, University of Toronto; Division of Molecular and Cellular Biology Research, Sunnybrook and Women's Research Institute, Toronto, Canada * Corresponding author; email: 130hama{at}nih.go.jp. Tie2 is a receptor type tyrosine kinase expressed on hematopoietic stem cells and endothelial cells. We utilized cultured ES cells to determine the function of Tie2 during early vascular development and hematopoiesis. Upon differentiation, the ES cell-derived Tie2+Flk1+ fraction was enriched for hematopoietic and endothelial progenitor cells. To investigate lymphatic differentiation, we used a monoclonal antibody against LYVE-1 and found that LYVE-1+ cells derived from Tie2+Flk1+ cells possessed various characteristics of lymphatic endothelial cells. To determine whether Tie2 played a role in this process, we analyzed differentiation of Tie2-/- ES cells. Although the initial numbers of LYVE-1+ and PECAM-1+ cells derived from Tie2-/- cells did not vary significantly, the number of both decreased dramatically upon extended culturing. Such decreases were rescued by treatment with a caspase inhibitor, suggesting that reductions were due to apoptosis as a consequence of a lack of Tie2 signaling. Interestingly, Tie2-/- ES cells did not show measurable defects in development of the hematopoietic system, suggesting that Tie2 is not essential for hematopoietic cell development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Voskas, Y. Babichev, L. S. Ling, J. Alami, Y. Shaked, R. S. Kerbel, B. Ciruna, and D. J. Dumont An eosinophil immune response characterizes the inflammatory skin disease observed in Tie-2 transgenic mice J. Leukoc. Biol., July 1, 2008; 84(1): 59 - 67. [Abstract] [Full Text] [PDF]

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