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Prepublished online as a Blood First Edition Paper on September 5, 2002; DOI 10.1182/blood-2002-05-1516. This Article Full Text (PDF) All Versions of this Article: 2002-05-1516v1 101/2/560    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 Oura, H. Articles by Detmar, M. Search for Related Content PubMed PubMed Citation Articles by Oura, H. Articles by Detmar, M. Social Bookmarking                   What's this? Submitted May 23, 2002 Accepted August 21, 2002 A critical role of placental growth factor in the induction of inflammation and edema formation Hajimu Oura, Jennifer Silva, Paula Velasco, Lawrence F Brown, Peter Carmeliet, and Michael Detmar* Cutaneous Biology Research Center and Department of Dermatology, Massachusetts General Hospital, Charlestown, MA, USA Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Center for Transgene Technology, University of Leuven, Leuven, Belgium * Corresponding author; email: michael.detmar{at}cbrc2.mgh.harvard.edu. Angiogenesis is a prominent feature of a number of inflammatory human diseases, including rheumatoid arthritis, psoriasis, and cutaneous delayed-type hypersensitivity (DTH) reactions. Upregulation of placental growth factor (PlGF), a member of the vascular endothelial growth factor (VEGF) family, has been found in several conditions associated with pathological angiogenesis; however, its distinct role in the control of angiogenesis has remained unclear. To directly investigate the biological function of PlGF in cutaneous inflammation and angiogenesis, DTH reactions were investigated in the ear skin of wild-type mice, of PlGF deficient mice, and of transgenic mice with targeted overexpression of human PlGF-2 in epidermal keratinocytes, driven by a keratin-14 promoter expression construct. Chronic transgenic delivery of PlGF-2 to murine epidermis resulted in a significantly increased inflammatory response, associated with more pronounced vascular enlargement, edema, and inflammatory cell infiltration than seen in wild-type mice. Conversely, PlGF deficiency resulted in a diminished and abbreviated inflammatory response, together with a reduction of inflammatory angiogenesis and edema formation. VEGF expression was upregulated at a comparable level in the inflamed skin of all genotypes. These findings reveal that placental growth factor plays a critical role in the control of cutaneous inflammation, and they suggest inhibition of PlGF bioactivity as a potential new approach for anti-inflammatory therapy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Patel, C. S. Gonsalves, M. Yang, P. Malik, and V. K. Kalra Placenta growth factor induces 5-lipoxygenase-activating protein to increase leukotriene formation in sickle cell disease Blood, January 29, 2009; 113(5): 1129 - 1138. [Abstract] [Full Text] [PDF] A. Cassidy, S. E. Chiuve, J. E. Manson, K. M. Rexrode, C. J. Girman, and E. B. 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	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020