Source:http://linkedlifedata.com/resource/pubmed/id/17690181
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0001554,
umls-concept:C0018787,
umls-concept:C0027051,
umls-concept:C0043240,
umls-concept:C0079459,
umls-concept:C0225360,
umls-concept:C0229601,
umls-concept:C0242767,
umls-concept:C0271510,
umls-concept:C0374711,
umls-concept:C1186763,
umls-concept:C1705181,
umls-concept:C1880177,
umls-concept:C2349975
|
pubmed:issue |
11
|
pubmed:dateCreated |
2007-11-8
|
pubmed:abstractText |
The administration of granulocyte colony-stimulating factor (G-CSF) after myocardial infarction (MI) improves cardiac function and survival rates in mice. It was also reported recently that bone marrow (BM)-derived c-kit(+) cells or macrophages in the infarcted heart are associated with improvement of cardiac remodeling and function. These observations prompted us to examine whether BM-derived hematopoietic cells mobilized by G-CSF administration after MI play a beneficial role in the infarct region. A single hematopoietic stem cell from green fluorescent protein (GFP)-transgenic mice was used to reconstitute hematopoiesis in each experimental mouse. MI was then induced, and the mice received G-CSF for 10 days. In the acute phase, a number of GFP(+) cells showing the elongated morphology were found in the infarcted area. Most of these cells were positive for vimentin and alpha-smooth muscle actin but negative for CD45, indicating that they were myofibroblasts. The number of these cells was markedly enhanced by G-CSF administration, and the enhanced myofibroblast-rich repair was considered to lead to improvements of cardiac remodeling, function, and survival rate. Next, G-CSF-mobilized monocytes were harvested from the peripheral blood of GFP-transgenic mice and injected intravenously into the infarcted mice. Following this procedure, GFP(+) myofibroblasts were observed in the infarcted myocardium. These results indicate that cardiac myofibroblasts are hematopoietic in origin and could arise from monocytes/macrophages. MI leads to the recruitment of monocytes, which differentiate into myofibroblasts in the infarct region. Administration of G-CSF promotes this recruitment and enhances cardiac protection.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
1549-4918
|
pubmed:author |
pubmed-author:AndoKiyoshiK,
pubmed-author:EndoJinJ,
pubmed-author:FujitaJunJ,
pubmed-author:FukudaKeiichiK,
pubmed-author:HottaTomomitsuT,
pubmed-author:IedaYasuyoY,
pubmed-author:KawadaHiroshiH,
pubmed-author:KawaguchiHarukoH,
pubmed-author:MatsuzakiYumiY,
pubmed-author:MoriMitsuharuM,
pubmed-author:OgawaSatoshiS,
pubmed-author:OkanoHideyukiH,
pubmed-author:TsumaMitsuyoM,
pubmed-author:YagiTakashiT,
pubmed-author:YozuRyoheiR,
pubmed-author:YuasaShinsukeS
|
pubmed:issnType |
Electronic
|
pubmed:volume |
25
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2750-9
|
pubmed:meshHeading |
pubmed-meshheading:17690181-Animals,
pubmed-meshheading:17690181-Fibroblasts,
pubmed-meshheading:17690181-Granulocyte Colony-Stimulating Factor,
pubmed-meshheading:17690181-Hematopoietic Stem Cells,
pubmed-meshheading:17690181-Mice,
pubmed-meshheading:17690181-Mice, Inbred C57BL,
pubmed-meshheading:17690181-Mice, Transgenic,
pubmed-meshheading:17690181-Myocardial Infarction,
pubmed-meshheading:17690181-Myocardium,
pubmed-meshheading:17690181-Regeneration,
pubmed-meshheading:17690181-Time Factors
|
pubmed:year |
2007
|
pubmed:articleTitle |
Administration of granulocyte colony-stimulating factor after myocardial infarction enhances the recruitment of hematopoietic stem cell-derived myofibroblasts and contributes to cardiac repair.
|
pubmed:affiliation |
Department of Regenerative Medicine and Advanced Cardiac Therapeutics, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan.
|
pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|