| pubmed-article:10205148 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C0162772 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C0600388 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:10205148 | lifeskim:mentions | umls-concept:C0439596 | lld:lifeskim |
| pubmed-article:10205148 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:10205148 | pubmed:dateCreated | 1999-4-30 | lld:pubmed |
| pubmed-article:10205148 | pubmed:abstractText | Endothelial cells (ECs) exposed to cyclic strain induce gene expression. To elucidate the signaling mechanisms involved, we studied the effects of cyclic strain on ECs by using early growth response-1 (Egr-1) as a target gene. Cyclic strain induced a transient increase of Egr-1 mRNA levels that resulted in an increase of binding of nuclear proteins to the Egr-1 binding sequences in the platelet-derived growth factor-A promoter region. ECs subjected to strain enhanced Egr-1 transcription as revealed by promoter activities. Catalase pretreatment inhibited this induction. ECs, transfected with a dominant positive mutant of Ras (RasL61), increased Egr-1 promoter activities. In contrast, transfection with a dominant negative mutant of Ras (RasN17) attenuated this strain inducibility. ECs transfected with a dominant negative mutant of Raf-1 (Raf301) or the catalytically inactive mutant of extracellular signal-regulated kinase (ERK)-2 (mERK2) diminished strain-induced promoter activities. However, little effect on strain inducibility was observed in ECs transfected with a dominant negative mutant of Rac (RacN17) or a catalytically inactive mutant of JNK (JNK[K-R]). Consistently, strain-induced Egr-1 expression was inhibited after ECs were treated with a specific inhibitor (PD98059) to mitogen-activated protein kinase kinase. Moreover, strain to ECs induced mitogen-activated protein kinase/ERK activity. The activation of the ERK pathway was further substantiated by an increase of strain-induced transcriptional activity of Elk1, an ERK substrate. This strain-induced ERK activity was attenuated after ECs were treated with N-acetylcysteine or catalase. Consequently, this Egr-1 gene induction was abolished after ECs were treated with N-acetylcysteine or catalase. Deletion analyses of the promoter region (-698 bp) indicated that cyclic strain and H2O2 shared a common serum response element. Our data clearly indicate that cyclic strain-induced Egr-1 expression is mediated mainly via the Ras/Raf-1/ERK pathway and that strain-induced reactive oxygen species can modulate Egr-1 expression at least partially via this signaling pathway. | lld:pubmed |
| pubmed-article:10205148 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10205148 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205148 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10205148 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10205148 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10205148 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10205148 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10205148 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:10205148 | pubmed:issn | 0009-7330 | lld:pubmed |
| pubmed-article:10205148 | pubmed:author | pubmed-author:WangD LDL | lld:pubmed |
| pubmed-article:10205148 | pubmed:author | pubmed-author:ChengJ JJJ | lld:pubmed |
| pubmed-article:10205148 | pubmed:author | pubmed-author:ChauY PYP | lld:pubmed |
| pubmed-article:10205148 | pubmed:author | pubmed-author:HsiehH JHJ | lld:pubmed |
| pubmed-article:10205148 | pubmed:author | pubmed-author:WungB SBS | lld:pubmed |
| pubmed-article:10205148 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10205148 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:10205148 | pubmed:volume | 84 | lld:pubmed |
| pubmed-article:10205148 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10205148 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10205148 | pubmed:pagination | 804-12 | lld:pubmed |
| pubmed-article:10205148 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10205148 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10205148 | pubmed:articleTitle | Modulation of Ras/Raf/extracellular signal-regulated kinase pathway by reactive oxygen species is involved in cyclic strain-induced early growth response-1 gene expression in endothelial cells. | lld:pubmed |
| pubmed-article:10205148 | pubmed:affiliation | Cardiovascular Division, Institute of Biomedical Sciences, Academia Sinica, and Department of Chemical Engineering, National Taiwan University, Taipei, Taiwan, ROC. | lld:pubmed |
| pubmed-article:10205148 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10205148 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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