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Prepublished online as a Blood First Edition Paper on April 24, 2003; DOI 10.1182/blood-2002-11-3422. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-11-3422v1 102/4/1506    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 Citing Articles via Google Scholar Google Scholar Articles by Perelman, N. Articles by Malik, P. Search for Related Content PubMed PubMed Citation Articles by Perelman, N. Articles by Malik, P. Related Collections Hemostasis, Thrombosis, and Vascular Biology Phagocytes Red Cells Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 August 2003, Vol. 102, No. 4, pp. 1506-1514 RED CELLS Placenta growth factor activates monocytes and correlates with sickle cell disease severity Natalya Perelman, Suresh K. Selvaraj, Sandeep Batra, Lori R. Luck, Anat Erdreich-Epstein, Thomas D. Coates, Vijay K. Kalra, and Punam Malik From the Division of Hematology-Oncology, Childrens Hospital Los Angeles; Departments of Pediatrics, Pathology, and Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California. Sickle cell disease (SCD) results in chronic hypoxia and secondarily increased erythropoietin concentrations. Leukocytosis and activated monocytes are also observed in SCD in absence of infection or vaso-occlusion (steady state), the reasons for which are unknown. We found that erythroid cells produced placenta growth factor (PlGF), an angiogenic growth factor belonging to the vascular endothelial growth factor (VEGF) family, and its expression was induced in bone marrow CD34+ progenitor cells in the presence of erythropoietin. Furthermore, the steady state circulating PlGF levels in subjects with severe SCD (at least 3 vaso-occlusive crises [VOCs] per year) were 18.5 ± 1.2 pg/mL (n = 9) compared with 15.5 ± 1.2 pg/mL (n = 13) in those with mild SCD (fewer than 3 VOCs per year) and 11.3 ± 0.7 pg/mL (n = 9) in healthy controls (P < .05), suggesting a correlation between PlGF levels and SCD severity. In addition, PlGF significantly increased mRNA levels of the proinflammatory cytochemokines interleukin-1, interleukin-8, monocyte chemoattractant protein-1, and VEGF in peripheral blood mononuclear cells (MNCs) of healthy subjects (n = 4; P < .05). Expression of these same cytochemokines was significantly increased in MNCs from subjects with SCD at steady state (n = 14), compared with healthy controls. Of the leukocyte subfractions, PlGF stimulated monocyte chemotaxis (P < .05, n = 3). Taken together, these data show for the first time that erythroid cells intrinsically release a factor that can directly activate monocytes to increase inflammation. The baseline inflammation seen in SCD has always been attributed to sequelae secondary to the sickling phenomenon. We show that PlGF contributes to the inflammation observed in SCD and increases the incidence of vaso-occlusive events. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: PlGF: a link between inflammation and angiogenesis in sickle disease Gregory M. Vercellotti Blood 2003 102: 1153. [Full Text] [PDF] This article has been cited by other articles: A. Hryniewicz-Jankowska, P. K. Choudhary, L. P. Ammann, C. T. Quinn, and S. R. Goodman Monocyte Protein Signatures of Disease Severity in Sickle Cell Anemia Experimental Biology and Medicine, February 1, 2009; 234(2): 210 - 221. [Abstract] [Full Text] [PDF] 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] K. Yano, Y. Okada, G. Beldi, S.-C. Shih, N. Bodyak, H. Okada, P. M. Kang, W. Luscinskas, S. C. Robson, P. Carmeliet, et al. Elevated levels of placental growth factor represent an adaptive host response in sepsis J. Exp. Med., October 27, 2008; 205(11): 2623 - 2631. [Abstract] [Full Text] [PDF] M. J. Telen It really IS the red cell Blood, August 1, 2008; 112(3): 459 - 460. [Full Text] [PDF] N. Patel, C. S. Gonsalves, P. Malik, and V. K. 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MURPHY Loss of metal transcription factor-1 suppresses tumor growth through enhanced matrix deposition FASEB J, August 1, 2004; 18(11): 1176 - 1184. [Abstract] [Full Text] [PDF] S. K. Selvaraj, R. K. Giri, N. Perelman, C. Johnson, P. Malik, and V. K. Kalra Mechanism of monocyte activation and expression of proinflammatory cytochemokines by placenta growth factor Blood, August 15, 2003; 102(4): 1515 - 1524. [Abstract] [Full Text] [PDF]

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