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Blood, 15 September 2006, Vol. 108, No. 6, pp. 1821-1829. Prepublished online as a Blood First Edition Paper on May 16, 2006; DOI 10.1182/blood-2005-10-009191. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2005-10-009191v1 108/6/1821    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 Kim, J.-S. Articles by Park, J.-B. Search for Related Content PubMed PubMed Citation Articles by Kim, J.-S. Articles by Park, J.-B. Related Collections Phagocytes Cell Adhesion and Motility Cytoskeleton Signal Transduction Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS Transforming growth factor-1 regulates macrophage migration via RhoA Jun-Sub Kim, Jae-Gyu Kim, Mi-Young Moon, Chan-Young Jeon, Ha-Young Won, Hee-Jun Kim, Yee-Jin Jeon, Ji-Yeon Seo, Jong-Il Kim, Jaebong Kim, Jae-Yong Lee, Pyeung-Hyeun Kim, and Jae-Bong Park From the Department of Biochemistry, College of Medicine, Hallym University, and the Department of Molecular Bioscience, School of Bioscience and Biotechnology, Kangwon National University, Chuncheon, Kangwon-Do, Korea. Brief treatment with transforming growth factor (TGF)–1 stimulated the migration of macrophages, whereas long-term exposure decreased their migration. Cell migration stimulated by TGF-1 was markedly inhibited by 10 µg/mL Tat-C3 exoenzyme. TGF-1 increased mRNA and protein levels of macrophage inflammatory protein (MIP)–1 in the initial period, and these effects also were inhibited by 10 µg/mL Tat-C3 and a dominant-negative (DN)–RhoA (N19RhoA). Cycloheximide, actinomycin D, and antibodies against MIP-1 and monocyte chemoattractant protein-1 (MCP-1) abolished the stimulation of cell migration by TGF-1. These findings suggest that migration of these cells is regulated directly and indirectly via the expression of chemokines such as MIP-1 and MCP-1 mediated by RhoA in response to TGF-1. TGF-1 activated RhoA in the initial period, and thereafter inactivated them, suggesting that the inactivation of RhoA may be the cause of the reduced cell migration in response to TGF-1 at later times. We therefore attempted to elucidate the molecular mechanism of the inactivation of RhoA by TGF-1. First, TGF-1 phosphorylated RhoA via protein kinase A, leading to inactivation of RhoA. Second, wild-type p190 Rho GTPase activating protein (p190RhoGAP) reduced and DN-p190RhoGAP reversed the reduction of cell migration induced by TGF-, suggesting that it inactivated RhoA via p190 Rho GAP. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: W. Jiang, M. Betson, R. Mulloy, R. Foster, M. Levay, E. Ligeti, and J. Settleman p190A RhoGAP Is a Glycogen Synthase Kinase-3-{beta} Substrate Required for Polarized Cell Migration J. Biol. Chem., July 25, 2008; 283(30): 20978 - 20988. [Abstract] [Full Text] [PDF] P. Holvoet and P. Sinnaeve Angio-Associated Migratory Cell Protein and Smooth Muscle Cell Migration in Development of Restenosis and Atherosclerosis J. Am. Coll. Cardiol., July 22, 2008; 52(4): 312 - 314. [Full Text] [PDF] G Ferraccioli and G Romano Renal interstitial cells, proteinuria and progression of lupus nephritis: new frontiers for old factors Lupus, June 1, 2008; 17(6): 533 - 540. [Abstract] [PDF]

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