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Related Collections Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 November 2001, Vol. 98, No. 9, pp. 2869-2871 BRIEF REPORT Syk expression in endothelial cells and their morphologic defects in embryonic Syk-deficient mice Shigeru Yanagi, Ryoko Inatome, Junyi Ding, Hironori Kitaguchi, Victor L. J. Tybulewicz, and Hirohei Yamamura From the Departments of Biochemistry and Physiology, Kobe University School of Medicine, Chuo-ku, Japan; and National Institute for Medical Research, London, United Kingdom. Mice deficient in the Syk tyrosine kinase showed severe petechiae in utero and died shortly after birth. The mechanism of this bleeding, however, remains unknown. Here it is shown that this bleeding is caused by morphologic defects of Syk-deficient endothelial cells during embryogenesis. Immunoblot and reverse transcriptase-polymerase chain reaction Northern blot analysis indicated that Syk is expressed in several endothelial cell lines. Immunocytochemical analysis also confirmed that Syk is expressed in the normal embryonic endothelial cells and is absent in Syk-deficient mice. Furthermore, electron microscopic analysis of Syk-deficient mice revealed an abnormal morphogenesis and a decreased number of endothelial cells. The results indicate a critical role for Syk in endothelial cell function and in maintaining vascular integrity in vivo. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Tohyama and H. Yamamura Protein Tyrosine Kinase, Syk: A Key Player in Phagocytic Cells J. Biochem., March 1, 2009; 145(3): 267 - 273. [Abstract] [Full Text] [PDF] K. M. Bijli, F. Fazal, M. Minhajuddin, and A. 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