Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:20154257rdf:typepubmed:Citationlld:pubmed
pubmed-article:20154257lifeskim:mentionsumls-concept:C0005953lld:lifeskim
pubmed-article:20154257lifeskim:mentionsumls-concept:C0151744lld:lifeskim
pubmed-article:20154257lifeskim:mentionsumls-concept:C1257975lld:lifeskim
pubmed-article:20154257lifeskim:mentionsumls-concept:C1514559lld:lifeskim
pubmed-article:20154257lifeskim:mentionsumls-concept:C0538674lld:lifeskim
pubmed-article:20154257lifeskim:mentionsumls-concept:C1280500lld:lifeskim
pubmed-article:20154257lifeskim:mentionsumls-concept:C0205374lld:lifeskim
pubmed-article:20154257pubmed:issue5lld:pubmed
pubmed-article:20154257pubmed:dateCreated2010-5-5lld:pubmed
pubmed-article:20154257pubmed:abstractTextAlthough mesenchymal stem cells (MSCs) have therapeutic potential for tissue injury, intolerance and poor cell viability limit their reparative capability. Therefore, we examined the impact of bone marrow-derived MSCs, in which heme oxygenase-1 (HO-1) was transiently overexpressed, on the repair of an ischemic myocardial injury. When MSCs and HO-1-overexpressed MSCs (MSC(HO-1)) were exposed to serum deprivation/hypoxia or H(2)O(2)-induced oxidative stress, MSC(HO-1) exhibited increased resistance to cell apoptosis compared with MSCs (17 +/- 1 vs. 30 +/- 2%, P < 0.05) and were markedly resistant to cell death (2 +/- 1 vs. 32 +/- 2%, P < 0.05). Under these conditions, vascular endothelial growth factor (VEGF) production was 2.1-fold greater in MSC(HO-1) than in MSCs. Pretreatment of MSCs and MSC(HO-1) with phosphatidylinositol 3-kinase (PI 3-kinase)/protein kinase B (Akt) pathway inhibitors such as LY-294002 (50 muM) or wortmannin (100 nM) significantly decreased VEGF production. In a rat infarction model with MSCs or MSC(HO-1) (5 x 10(6) +/- 0.1 x 10(6) cells/rat) transplantation, the number of TdT-mediated dUTP nick end-labeling-positive cells was significantly lower in the MSC(HO-1) group than in the MSC group (12.1 +/- 1.0 cells/field vs. 26.5 +/- 2.6, P < 0.05) on the 4th day after cell transplantation. On the 28th day, increased capillary density associated with decreased infarction size was observed in the MSC(HO-1) group (1,415 +/- 47/mm(2) with 21.6 +/- 2.3%) compared with those in the MSCs group (1,215 +/- 43/mm(2) with 28.2 +/- 2.3%, P < 0.05), although infarction size relative to area at risk was not different in each group at 24 h after transplantation. These results demonstrate that MSC(HO-1) exhibit markedly enhanced anti-apoptotic and anti-oxidative capabilities compared with MSCs, thus contributing to improved repair of ischemic myocardial injury through cell survival and VEGF production associated with the PI 3-kinase/Akt pathway.lld:pubmed
pubmed-article:20154257pubmed:languageenglld:pubmed
pubmed-article:20154257pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:citationSubsetIMlld:pubmed
pubmed-article:20154257pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:20154257pubmed:statusMEDLINElld:pubmed
pubmed-article:20154257pubmed:monthMaylld:pubmed
pubmed-article:20154257pubmed:issn1522-1539lld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:FujinoNoboruNlld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:InoHidekazuHlld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:KonnoTetsuoTlld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:NagayaNoritos...lld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:YamagishiMasa...lld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:Ishibashi-Ued...lld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:NoharaAtsushi...lld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:YagiKunimasaKlld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:KawashiriMasa...lld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:ZukaMasahikoMlld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:TsubokawaTosh...lld:pubmed
pubmed-article:20154257pubmed:authorpubmed-author:NakanishiChia...lld:pubmed
pubmed-article:20154257pubmed:issnTypeElectroniclld:pubmed
pubmed-article:20154257pubmed:volume298lld:pubmed
pubmed-article:20154257pubmed:ownerNLMlld:pubmed
pubmed-article:20154257pubmed:authorsCompleteYlld:pubmed
pubmed-article:20154257pubmed:paginationH1320-9lld:pubmed
pubmed-article:20154257pubmed:dateRevised2010-11-18lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:meshHeadingpubmed-meshheading:20154257...lld:pubmed
pubmed-article:20154257pubmed:year2010lld:pubmed
pubmed-article:20154257pubmed:articleTitleImpact of anti-apoptotic and anti-oxidative effects of bone marrow mesenchymal stem cells with transient overexpression of heme oxygenase-1 on myocardial ischemia.lld:pubmed
pubmed-article:20154257pubmed:affiliationDivision of Cardiovascular Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, Japan.lld:pubmed
pubmed-article:20154257pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20154257pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
entrez-gene:24451entrezgene:pubmedpubmed-article:20154257lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:20154257lld:entrezgene
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:20154257lld:pubmed