| pubmed-article:17328891 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17328891 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:17328891 | lifeskim:mentions | umls-concept:C1704256 | lld:lifeskim |
| pubmed-article:17328891 | lifeskim:mentions | umls-concept:C0227651 | lld:lifeskim |
| pubmed-article:17328891 | lifeskim:mentions | umls-concept:C1166758 | lld:lifeskim |
| pubmed-article:17328891 | lifeskim:mentions | umls-concept:C0030190 | lld:lifeskim |
| pubmed-article:17328891 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:17328891 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:17328891 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17328891 | pubmed:dateCreated | 2007-3-23 | lld:pubmed |
| pubmed-article:17328891 | pubmed:abstractText | The importance of transforming growth factor-beta1 (TGF-beta1) in plasminogen activator inhibitor-1 (PAI-1) gene expression has been established, but the precise intracellular mechanisms are not fully understood. Our hypothesis is that the actin cytoskeleton is involved in TGF-beta1/MAPK-mediated PAI-1 expression in human mesangial cells. Examination of the distributions of actin filaments (F-actin), alpha-actinin, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by immunofluorescence and immunoprecipitation revealed that ERK and JNK associate with alpha-actinin along F-actin and that TGF-beta1 stimulation promote the dissociation of ERK and JNK with F-actin. Disassembly of the actin cytoskeleton inhibited phosphorylation of ERK and JNK and modulated PAI-1 expression and promoter activity under both basal and TGF-beta1-stimulated conditions. Stabilizing actin prevented dephosphorylation of ERK and JNK. ERK and JNK inhibitors and overexpressed dominant negative mutants antagonized the ability of TGF-beta1 to increase PAI-1 expression and promoter activity. Disassembly of F-actin also inhibited AP-1 DNA binding activity as determined by electrophoretic mobility shift assay using AP-1 consensus oligonucleotides derived from human PAI-1 promoter. F-actin stabilization prevented loss of AP-1 DNA binding activity. Therefore, changes in actin cytoskeleton modulate the ability of TGF-beta1 to stimulate PAI-1 expression through a mechanism dependent on the activation of MAPK/AP-1 pathways. | lld:pubmed |
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| pubmed-article:17328891 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17328891 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17328891 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17328891 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:17328891 | pubmed:issn | 0014-4827 | lld:pubmed |
| pubmed-article:17328891 | pubmed:author | pubmed-author:GlassWilliam... | lld:pubmed |
| pubmed-article:17328891 | pubmed:author | pubmed-author:PatelKeyurK | lld:pubmed |
| pubmed-article:17328891 | pubmed:author | pubmed-author:ChenYangY | lld:pubmed |
| pubmed-article:17328891 | pubmed:author | pubmed-author:SorokinAndrey... | lld:pubmed |
| pubmed-article:17328891 | pubmed:author | pubmed-author:HardingPamela... | lld:pubmed |
| pubmed-article:17328891 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17328891 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17328891 | pubmed:volume | 313 | lld:pubmed |
| pubmed-article:17328891 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17328891 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17328891 | pubmed:pagination | 1240-50 | lld:pubmed |
| pubmed-article:17328891 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:17328891 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17328891 | pubmed:articleTitle | Regulation of TGF-beta1/MAPK-mediated PAI-1 gene expression by the actin cytoskeleton in human mesangial cells. | lld:pubmed |
| pubmed-article:17328891 | pubmed:affiliation | Department of Pathology and Anatomy, Eastern Virginia Medical School, Norfolk, VA 23501, USA. chenyang@mcw.edu | lld:pubmed |
| pubmed-article:17328891 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17328891 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17328891 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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