pubmed-article:20154257 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20154257 | lifeskim:mentions | umls-concept:C0005953 | lld:lifeskim |
pubmed-article:20154257 | lifeskim:mentions | umls-concept:C0151744 | lld:lifeskim |
pubmed-article:20154257 | lifeskim:mentions | umls-concept:C1257975 | lld:lifeskim |
pubmed-article:20154257 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
pubmed-article:20154257 | lifeskim:mentions | umls-concept:C0538674 | lld:lifeskim |
pubmed-article:20154257 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:20154257 | lifeskim:mentions | umls-concept:C0205374 | lld:lifeskim |
pubmed-article:20154257 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:20154257 | pubmed:dateCreated | 2010-5-5 | lld:pubmed |
pubmed-article:20154257 | pubmed:abstractText | Although 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:20154257 | pubmed:language | eng | lld:pubmed |
pubmed-article:20154257 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20154257 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20154257 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20154257 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:20154257 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20154257 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20154257 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20154257 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20154257 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20154257 | pubmed:month | May | lld:pubmed |
pubmed-article:20154257 | pubmed:issn | 1522-1539 | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:FujinoNoboruN | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:InoHidekazuH | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:KonnoTetsuoT | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:NagayaNoritos... | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:YamagishiMasa... | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:Ishibashi-Ued... | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:NoharaAtsushi... | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:YagiKunimasaK | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:KawashiriMasa... | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:ZukaMasahikoM | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:TsubokawaTosh... | lld:pubmed |
pubmed-article:20154257 | pubmed:author | pubmed-author:NakanishiChia... | lld:pubmed |
pubmed-article:20154257 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20154257 | pubmed:volume | 298 | lld:pubmed |
pubmed-article:20154257 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20154257 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20154257 | pubmed:pagination | H1320-9 | lld:pubmed |
pubmed-article:20154257 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:20154257 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20154257 | pubmed:articleTitle | Impact 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:20154257 | pubmed:affiliation | Division of Cardiovascular Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, Japan. | lld:pubmed |
pubmed-article:20154257 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20154257 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:24451 | entrezgene:pubmed | pubmed-article:20154257 | lld:entrezgene |
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