| pubmed-article:18277950 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18277950 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:18277950 | lifeskim:mentions | umls-concept:C0232164 | lld:lifeskim |
| pubmed-article:18277950 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:18277950 | lifeskim:mentions | umls-concept:C0017911 | lld:lifeskim |
| pubmed-article:18277950 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:18277950 | lifeskim:mentions | umls-concept:C1882115 | lld:lifeskim |
| pubmed-article:18277950 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:18277950 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:18277950 | pubmed:dateCreated | 2008-9-22 | lld:pubmed |
| pubmed-article:18277950 | pubmed:abstractText | Both p38 mitogen-activated protein kinase (p38) activation and protein kinase B (Akt) activation have been reported to regulate glucose transport during myocardial I/R. An increase in cardiac glycogen levels prevents myocardial injury in the ischemic or stressed heart. Although studies have shown that 17"-estradiol (E2)-mediated improvement in cardiac function after trauma-hemorrhage is via p38 activation, it remains unknown whether p38/Akt plays any role in regulation of cardiac glycogen levels under these conditions. To study this, male rats underwent trauma-hemorrhage(mean blood pressure, x40 mmHg for 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats (n=6 per group) were treated with vehicle, E2 (1 mg/kg body weight), the p38 inhibitor SB203580 (2 mg/kg body weight), or E2 and SB203580. Various parameters were measured at 2 h after resuscitation. One-way ANOVA and Tukey test were used for statistical analysis, and differences were considered significant at P<0.05. The depressed cardiac function after trauma-hemorrhage was restored by E2 treatment (P<0.05). Administration of E2 after trauma-hemorrhage also normalized the p38/Akt phosphorylation, which was associated with restoration of cardiac glycogen, glycogen synthase kinase 3"activation, glucose transporter 4 translocation, and increased hexokinase II levels (all parameters, P<0.05). Inhibition of the p38 pathway abolished the E2-induced restoration in above parameters after trauma-hemorrhage. These results suggest that p38-dependent normalization of cardiac Akt phosphorylation and glycogen levels plays an important role in E2-mediated restoration of cardiac function after trauma-hemorrhage. | lld:pubmed |
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| pubmed-article:18277950 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18277950 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18277950 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18277950 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18277950 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18277950 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18277950 | pubmed:issn | 1540-0514 | lld:pubmed |
| pubmed-article:18277950 | pubmed:author | pubmed-author:SchwachaMarti... | lld:pubmed |
| pubmed-article:18277950 | pubmed:author | pubmed-author:BlandKirby... | lld:pubmed |
| pubmed-article:18277950 | pubmed:author | pubmed-author:ChaudryIrshad... | lld:pubmed |
| pubmed-article:18277950 | pubmed:author | pubmed-author:HsiehYa-Ching... | lld:pubmed |
| pubmed-article:18277950 | pubmed:author | pubmed-author:KanWen-HongWH | lld:pubmed |
| pubmed-article:18277950 | pubmed:author | pubmed-author:ChoudhryMashk... | lld:pubmed |
| pubmed-article:18277950 | pubmed:author | pubmed-author:HsuJun-TeJT | lld:pubmed |
| pubmed-article:18277950 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18277950 | pubmed:volume | 30 | lld:pubmed |
| pubmed-article:18277950 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18277950 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18277950 | pubmed:pagination | 372-8 | lld:pubmed |
| pubmed-article:18277950 | pubmed:dateRevised | 2010-2-22 | lld:pubmed |
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| pubmed-article:18277950 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18277950 | pubmed:articleTitle | Mechanism of estrogen-mediated improvement in cardiac function after trauma-hemorrhage: p38-dependent normalization of cardiac Akt phosphorylation and glycogen levels. | lld:pubmed |
| pubmed-article:18277950 | pubmed:affiliation | Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama 35294-0019, USA. | lld:pubmed |
| pubmed-article:18277950 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18277950 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18277950 | lld:pubmed |
