Source:http://linkedlifedata.com/resource/pubmed/id/20154257
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2010-5-5
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| 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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Serum-Free,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase-1,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt,
http://linkedlifedata.com/resource/pubmed/chemical/RNA,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A
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| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
1522-1539
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| pubmed:author |
pubmed-author:FujinoNoboruN,
pubmed-author:InoHidekazuH,
pubmed-author:Ishibashi-UedaHatsueH,
pubmed-author:KawashiriMasa-akiMA,
pubmed-author:KonnoTetsuoT,
pubmed-author:NagayaNoritoshiN,
pubmed-author:NakanishiChiakiC,
pubmed-author:NoharaAtsushiA,
pubmed-author:TsubokawaToshinariT,
pubmed-author:YagiKunimasaK,
pubmed-author:YamagishiMasakazuM,
pubmed-author:ZukaMasahikoM
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| pubmed:issnType |
Electronic
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| pubmed:volume |
298
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
H1320-9
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:20154257-Animals,
pubmed-meshheading:20154257-Apoptosis,
pubmed-meshheading:20154257-Bone Marrow Transplantation,
pubmed-meshheading:20154257-Capillaries,
pubmed-meshheading:20154257-Cell Differentiation,
pubmed-meshheading:20154257-Cell Lineage,
pubmed-meshheading:20154257-Cell Survival,
pubmed-meshheading:20154257-Culture Media, Serum-Free,
pubmed-meshheading:20154257-Cytokines,
pubmed-meshheading:20154257-Heme Oxygenase-1,
pubmed-meshheading:20154257-Male,
pubmed-meshheading:20154257-Mesenchymal Stem Cell Transplantation,
pubmed-meshheading:20154257-Myocardial Ischemia,
pubmed-meshheading:20154257-Oxidative Stress,
pubmed-meshheading:20154257-Phenotype,
pubmed-meshheading:20154257-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:20154257-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:20154257-RNA,
pubmed-meshheading:20154257-Rats,
pubmed-meshheading:20154257-Rats, Inbred Lew,
pubmed-meshheading:20154257-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20154257-Vascular Endothelial Growth Factor A
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| pubmed:year |
2010
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| 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.
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| pubmed:affiliation |
Division of Cardiovascular Medicine, Kanazawa University Graduate School of Medicine, Takara-machi 13-1, Kanazawa, Ishikawa, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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