| pubmed-article:18298650 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18298650 | lifeskim:mentions | umls-concept:C0023977 | lld:lifeskim |
| pubmed-article:18298650 | lifeskim:mentions | umls-concept:C0079459 | lld:lifeskim |
| pubmed-article:18298650 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:18298650 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:18298650 | lifeskim:mentions | umls-concept:C1522240 | lld:lifeskim |
| pubmed-article:18298650 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:18298650 | pubmed:dateCreated | 2008-9-10 | lld:pubmed |
| pubmed-article:18298650 | pubmed:abstractText | Although beneficial effects of granulocyte colony-stimulating factor (G-CSF) have been demonstrated on post-myocardia infarction (MI) process, the mechanisms and feasibility are not fully agreed yet. We investigated effects of a long-term treatment with a low-dose G-CSF started 1 day after the onset of MI, on post-infarction process. One day after being made MI by left coronary ligation, mice were given G-CSF (10 microg/kg/day) for 4 weeks. The G-CSF treatment resulted in a significant mitigation of cardiac remodelling and dysfunction. In the G-CSF-treated hearts, the infarcted scar was smaller with less fibrosis and abundant vessels while in the non-infarcted area, hypertrophic cardiomyocytes with attenuated degenerative changes and reduced fibrosis were apparent. These effects were accompanied by activation of signal transducer and activator of transcription 3 (STAT3) and Akt and also by up-regulation of GATA-4, myosin heavy chain and matrix metalloproteinases-2 and -9. Apoptosis of cardiomyocytes appeared insignificant at any stages. Parthenolide, a STAT3 inhibitor, completely abolished the beneficial effects of G-CSF on cardiac function and remodelling with loss of effect on both anti-cardiomyocyte degeneration and anti-fibrosis. In contrast, wortmannin, an Akt inhibitor, did not affect G-CSF-induced benefits despite cancelling vessel increase. In conclusion, treatment with G-CSF at a small dose but for a long duration beneficially affects the post-infarction process possibly through STAT3-mediated anti-cardiomyocyte degeneration and anti-fibrosis, but not through anti-cardiomyocyte apoptosis or Akt-mediated angio-genesis. The findings may also imply a more feasible way of G-CSF administration in the clinical settings. | lld:pubmed |
| pubmed-article:18298650 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18298650 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18298650 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18298650 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18298650 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:18298650 | pubmed:issn | 1582-1838 | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:OhnoTakamasaT | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:MinatoguchiSh... | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:FujiwaraHisay... | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:MaruyamaRumiR | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:TakemuraGenzo... | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:FujiwaraTakak... | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:LiYiwenY | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:EsakiMasayasu... | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:OkadaHideshiH | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:OginoAtsushiA | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:MiyataShusaku... | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:KanamoriHirom... | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:LiLonghuL | lld:pubmed |
| pubmed-article:18298650 | pubmed:author | pubmed-author:NakagawaMuneh... | lld:pubmed |
| pubmed-article:18298650 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18298650 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:18298650 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18298650 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18298650 | pubmed:pagination | 1272-83 | lld:pubmed |
| pubmed-article:18298650 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:18298650 | pubmed:meshHeading | pubmed-meshheading:18298650... | lld:pubmed |
| pubmed-article:18298650 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18298650 | pubmed:articleTitle | Effect of a long-term treatment with a low-dose granulocyte colony-stimulating factor on post-infarction process in the heart. | lld:pubmed |
| pubmed-article:18298650 | pubmed:affiliation | Division of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan. | lld:pubmed |
| pubmed-article:18298650 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18298650 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
