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Prepublished online as a Blood First Edition Paper on April 10, 2003; DOI 10.1182/blood-2002-11-3423. This Article Full Text (PDF) All Versions of this Article: 2002-11-3423v1 102/4/1515    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 Selvaraj, S. K Articles by Kalra, V. K Search for Related Content PubMed PubMed Citation Articles by Selvaraj, S. K Articles by Kalra, V. K Related Collections Related Article in Blood Online Social Bookmarking                   What's this? Submitted November 12, 2002 Accepted March 31, 2003 Mechanism of monocyte activation and expression of proinflammatory cytochemokines by placenta growth factor Suresh K Selvaraj, Ranjit K Giri, Natalya Perelman, Cage Johnson, Punam Malik, and Vijay K Kalra* Biochemistry and Molecular Biology, University of Southern California, Keck School of Medicine, Los Angeles, CA, USA Division of Hematology - Oncology, Childrens Hospital, Los Angeles, CA, USA Medicine, University of Southern California, Keck School of Medicine, Los Angeles, CA, USA Pediatrics and Pathology, University of Southern California, Keck School of Medicine, Los Angeles, CA, USA * Corresponding author; email: vkalra{at}usc.edu. Monocytes from patients with sickle cell disease (SCD) are in an activated state. However, the mechanism of activation of monocytes in SCD is not known. Our studies showed that placenta growth factor (PlGF) activated monocytes and increased mRNA levels of cytokines (TNF- and IL-1) and chemokines (MCP-1, IL-8 and MIP-1) in both normal monocytes and in the THP-1 monocytic cell line. This increase in mRNA expression of cytochemokines was also reflected in monocytes derived from subjects with SCD. We studied the PlGF-mediated downstream cellular signaling events that caused increased transcription of inflammatory cytochemokines and monocyte chemotaxis. PlGF-mediated cytochemokine mRNA and protein expression was inhibited by PD98059 and Wortmannin, inhibitors of MEK kinase and PI3 kinase, respectively, but not by SB 203580, a p38 kinase inhibitor. PlGF caused a time dependent transient increase in phosphorylation of ERK-1/2, which was completely inhibited by Wortmannin, indicating that activation of PI3 kinase preceded MEK activation. PlGF also induced transient phosphorylation of AKT. Overexpression of a dominant-negative AKT or a dominant-negative PI3 kinase p85 subunit in THP-1 monocytes attenuated the PlGF-mediated phosphorylation of ERK-1/2, confirming that PlGF induced phosphorylation of ERK involves activation of PI3 kinase/AKT. MEK and PI3 kinase inhibitors also inhibited PlGF-induced chemotaxis of monocytes. Taken together, these data show that activation of monocytes by PlGF occurs via activation of PI3 kinase/AKT and ERK-1/2 pathways. Therefore, we propose that increased levels of PlGF in circulation play an important role in the inflammation observed in SCD via its effects on monocytes. 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: M. Markovic, S. Ignjatovic, N. Majkic-Singh, and M. 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