Abstract
In the process of atherosclerosis, platelet activating factor (PAF) promotes the infiltration of inflammatory cells into atherosclerotic plaque by modulating their cytoskeleton. Here, we examined whether Rho family proteins are involved in PAF-induced cytoskeletal reorganization in THP-1 macrophages. PAF stimulation rapidly induced cell elongation, accompanied by filopodia formation. The inhibition of Rho family proteins by the overexpression of Rho-GDI attenuated the PAF-mediated morphological changes. Both RhoA and Cdc42 were activated in response to PAF. Inhibition of RhoA or Cdc42 by dominant negative mutants abrogated morphological changes induced by PAF. Collectively, PAF regulates cytoarchitecture through Rho family proteins in macrophages.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenoviridae / genetics
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Arteriosclerosis / metabolism
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Cell Line, Tumor
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Cytoskeleton / metabolism*
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Gene Transfer Techniques
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Guanine Nucleotide Dissociation Inhibitors / metabolism
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Guanosine Triphosphate / chemistry
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Guanosine Triphosphate / metabolism
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Humans
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Immunoblotting
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Inflammation
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Macrophages / metabolism*
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Platelet Activating Factor / metabolism*
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Pseudopodia / metabolism
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Time Factors
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Up-Regulation
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beta-Galactosidase / metabolism
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cdc42 GTP-Binding Protein / metabolism
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rac1 GTP-Binding Protein / metabolism
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rho GTP-Binding Proteins / metabolism*
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rho-Specific Guanine Nucleotide Dissociation Inhibitors
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rhoA GTP-Binding Protein / metabolism
Substances
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Guanine Nucleotide Dissociation Inhibitors
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Platelet Activating Factor
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rho-Specific Guanine Nucleotide Dissociation Inhibitors
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Guanosine Triphosphate
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beta-Galactosidase
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cdc42 GTP-Binding Protein
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rac1 GTP-Binding Protein
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rho GTP-Binding Proteins
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rhoA GTP-Binding Protein