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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.
 Previous Article | Next Article 
Submitted October 18, 2005
Accepted April 28, 2006
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*
Department of Biochemistry, College of Medicine, Hallym University
Department of Molecular Bioscience, School of Bioscience & Biotechnology,Kangwon National University
* Corresponding author; email: jbpark{at}hallym.ac.kr.
Brief treatment with transforming growth factor (TGF)-
 1 stimulated the migration of macrophages, whereas
long-term exposure decreased their migration. Ten
µg/ml Tat-C3 exoenzyme markedly inhibited cell
migration stimulated by TGF-1. TGF- 1 increased mRNA
and protein levels of macrophage inflammatory protein
(MIP)-1 in the initial period, and these effects were
also inhibited by 10 µg/ml Tat-C3 and a dominant
negative 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
like 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, WT p190 Rho GTPase
activating protein (p190RhoGAP) reduced and DN-
p190RhoGAP reversed the reduction of cell migration by
TGF-, suggesting that it inactivated RhoA via
p190RhoGAP.
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