| pubmed-article:15681821 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15681821 | lifeskim:mentions | umls-concept:C0175677 | lld:lifeskim |
| pubmed-article:15681821 | lifeskim:mentions | umls-concept:C0040300 | lld:lifeskim |
| pubmed-article:15681821 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
| pubmed-article:15681821 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:15681821 | lifeskim:mentions | umls-concept:C1449702 | lld:lifeskim |
| pubmed-article:15681821 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:15681821 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:15681821 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15681821 | pubmed:dateCreated | 2005-1-31 | lld:pubmed |
| pubmed-article:15681821 | pubmed:abstractText | Progressive fibrotic diseases involving diverse organ systems are associated with the persistence of fibroblasts/myofibroblasts in injured tissues. Activation of focal adhesion kinase (FAK) and protein kinase B (PKB/Akt) by transforming growth factor-beta1 mediate stable induction of myofibroblast differentiation and survival. In this report, we demonstrate that transforming growth factor-beta1-induced activation of both PKB/Akt and FAK are dose dependently inhibited by the protein kinase inhibitor, AG1879, in cultured human lung fibroblasts. In a murine model of intratracheal bleomycin-induced lung fibrosis, regions of active fibrogenesis demonstrate elevated expression of PKB/Akt and FAK phosphorylation in vivo, effects that are attenuated in mice receiving daily intraperitoneal injections of AG1879 (bleomycin-AG1879) versus a chemically inactive analog (bleomycin-control). PKB/Akt and FAK phosphorylation are elevated in fibroblasts isolated from lungs of bleomycin-injured mice, effects that are inhibited in bleomycin-AG1879 mice. Accumulation of alpha-smooth muscle actin-expressing myofibroblasts is markedly reduced in lungs of bleomycin-AG1879 mice. The numbers of recruited inflammatory cells were not significantly different between these groups. Bleomycin-AG1879 mice are protected from lung fibrosis as evidenced by histopathology, trichrome staining, and biochemical analysis for collagen. Thus, targeting of prosurvival signaling pathways in fibroblasts/myofibroblasts may provide a novel and effective strategy for anti-fibrotic therapy of treatment-unresponsive fibrotic disorders. | lld:pubmed |
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| pubmed-article:15681821 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15681821 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:15681821 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15681821 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:15681821 | pubmed:issn | 0002-9440 | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:ToewsGalen... | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:StandifordThe... | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:MooreBethany... | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:MartinezFerna... | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:ThannickalVic... | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:HorowitzJeffr... | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:ZhangHengminH | lld:pubmed |
| pubmed-article:15681821 | pubmed:author | pubmed-author:VittalRaginiR | lld:pubmed |
| pubmed-article:15681821 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15681821 | pubmed:volume | 166 | lld:pubmed |
| pubmed-article:15681821 | pubmed:owner | NLM | lld:pubmed |
