SEARCH:   Advanced

Blood, 30 July 2009, Vol. 114, No. 5, pp. 1123-1130. Prepublished online as a Blood First Edition Paper on May 1, 2009; DOI 10.1182/blood-2009-03-211391. This Article Full Text Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2009-03-211391v1 114/5/1123    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Google Scholar Articles by Wei, G. Articles by Ostrowski, M. C. PubMed PubMed Citation Articles by Wei, G. Articles by Ostrowski, M. C. Related Collections Vascular Biology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  VASCULAR BIOLOGY Ets1 and Ets2 are required for endothelial cell survival during embryonic angiogenesis Guo Wei*,1,2, Ruchika Srinivasan*,1,2, Carmen Z. Cantemir-Stone1,2, Sudarshana M. Sharma1,2, Ramasamy Santhanam1,2, Michael Weinstein24, Natarajan Muthusamy2,5, Albert K. Man6, Robert G. Oshima6, Gustavo Leone24, and Michael C. Ostrowski1,2 1 Department of Molecular and Cellular Biochemistry, 2 The Comprehensive Cancer Center, 3 Division of Human Cancer Genetics, Department of Molecular Virology, Immunology and Medical Genetics, 4 Department of Molecular Genetics, and 5 Division of Hematology and Oncology, Department of Medicine, The Ohio State University, Columbus; and 6 Oncodevelopmental Biology Program, The Burnham Institute, La Jolla, CA The ras/Raf/Mek/Erk pathway plays a central role in coordinating endothelial cell activities during angiogenesis. Transcription factors Ets1 and Ets2 are targets of ras/Erk signaling pathways that have been implicated in endothelial cell function in vitro, but their precise role in vascular formation and function in vivo remains ill-defined. In this work, mutation of both Ets1 and Ets2 resulted in embryonic lethality at midgestation, with striking defects in vascular branching having been observed. The action of these factors was endothelial cell autonomous as demonstrated using Cre/loxP technology. Analysis of Ets1/Ets2 target genes in isolated embryonic endothelial cells demonstrated down-regulation of Mmp9, Bcl-XL, and cIAP2 in double mutants versus controls, and chromatin immunoprecipitation revealed that both Ets1 and Ets2 were loaded at target promoters. Consistent with these observations, endothelial cell apoptosis was significantly increased both in vivo and in vitro when both Ets1 and Ets2 were mutated. These results establish essential and overlapping functions for Ets1 and Ets2 in coordinating endothelial cell functions with survival during embryonic angiogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Functional redundancy of Ets1 and Ets2 Peter Oettgen Blood 2009 114: 934-935. [Abstract] [Full Text] [PDF] This article has been cited by other articles: P. Oettgen Functional redundancy of Ets1 and Ets2 Blood, July 30, 2009; 114(5): 934 - 935. [Abstract] [Full Text] [PDF]

	Copyright © 2009 by American Society of Hematology         Online ISSN: 1528-0020