| pubmed-article:17513782 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17513782 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17513782 | lifeskim:mentions | umls-concept:C0151744 | lld:lifeskim |
| pubmed-article:17513782 | lifeskim:mentions | umls-concept:C0031621 | lld:lifeskim |
| pubmed-article:17513782 | lifeskim:mentions | umls-concept:C0035126 | lld:lifeskim |
| pubmed-article:17513782 | lifeskim:mentions | umls-concept:C1545588 | lld:lifeskim |
| pubmed-article:17513782 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:17513782 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:17513782 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:17513782 | pubmed:dateCreated | 2007-5-21 | lld:pubmed |
| pubmed-article:17513782 | pubmed:abstractText | TLRs play a critical role in the induction of innate and adaptive immunity. However, TLRs have also been reported to mediate the pathophysiology of organ damage following ischemia/reperfusion (I/R) injury. We have reported that TLR4(-/-) mice show decreased myocardial injury following I/R; however, the protective mechanisms have not been elucidated. We examined the role of the PI3K/Akt signaling pathway in TLR4(-/-) cardioprotection following I/R injury. TLR4(-/-) and age-matched wild-type (WT) mice were subjected to myocardial ischemia for 45 min, followed by reperfusion for 4 h. Pharmacologic inhibitors of PI3K (wortmannin or LY294002) were administered 1 h before myocardial I/R. Myocardial infarct size/area at risk was reduced by 51.2% in TLR4(-/-) vs WT mice. Cardiac myocyte apoptosis was also increased in WT vs TLR4(-/-) mice following I/R. Pharmacologic blockade of PI3K abrogated myocardial protection in TLR4(-/-) mice following I/R. Specifically, heart infarct size/area at risk was increased by 98% in wortmannin and 101% in LY294002-treated TLR4(-/-) mice, when compared with control TLR4(-/-) mice. These data indicate that protection against myocardial I/R injury in TLR4(-/-) mice is mediated through a PI3K/Akt-dependent mechanism. The mechanisms by which PI3K/Akt are increased in the TLR4(-/-) myocardium may involve increased phosphorylation/inactivation of myocardial phosphatase and tensin homolog deleted on chromosome 10 as well as increased phosphorylation/inactivation of myocardial glycogen synthase kinase-3beta. These data implicate innate immune signaling pathways in the pathology of acute myocardial I/R injury. These data also suggest that modulation of TLR4/PI3K/Akt-dependent signaling pathways may be a viable strategy for reducing myocardial I/R injury. | lld:pubmed |
| pubmed-article:17513782 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17513782 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17513782 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17513782 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17513782 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:17513782 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17513782 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17513782 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:17513782 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:LiYanY | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:MaJingJ | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:WilliamsDavid... | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:GaoXiangX | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:KelleyJimJ | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:LiChuanfuC | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:BrowderI... | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:HuaFangF | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:HaTuanzhuT | lld:pubmed |
| pubmed-article:17513782 | pubmed:author | pubmed-author:KaoRace LRL | lld:pubmed |
| pubmed-article:17513782 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17513782 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17513782 | pubmed:volume | 178 | lld:pubmed |
| pubmed-article:17513782 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17513782 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17513782 | pubmed:pagination | 7317-24 | lld:pubmed |
| pubmed-article:17513782 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:17513782 | pubmed:meshHeading | pubmed-meshheading:17513782... | lld:pubmed |
| pubmed-article:17513782 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17513782 | pubmed:articleTitle | Protection against myocardial ischemia/reperfusion injury in TLR4-deficient mice is mediated through a phosphoinositide 3-kinase-dependent mechanism. | lld:pubmed |
| pubmed-article:17513782 | pubmed:affiliation | Department of Surgery, East Tennessee State University, Johnson City, TN 37614, USA. | lld:pubmed |
| pubmed-article:17513782 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17513782 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17513782 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:21898 | entrezgene:pubmed | pubmed-article:17513782 | lld:entrezgene |
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