Source:http://linkedlifedata.com/resource/pubmed/id/14667198
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2003-12-11
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pubmed:abstractText |
To investigate the relationship between c-kit expression and cell cycle regulation by endogenous transforming growth factor-beta (TGF-beta) in human bone marrow hematopoietic progenitor cells, CD34+ CD38- c-kit(low/-) and CD34+ CD38- c-kit(high) populations were cultured in stem cell factor, thrombopoietin, interleukin-3 (IL-3), IL-6, granulocyte colony-stimulating factor, granulocyte/macrophage colony-stimulating factor and anti-TGF-beta, and analyzed for cell cycle status. Arrest in G0/G1 was most prominent in the precultured CD34+ CD38- c-kit(low/-) subset (95.62 +/- 4.15%). While postcultured CD34+ CD38- c-kit(high) cells initiated from CD34+ CD38- c-kit(high) cells entered cell cycle within 36 hr, postcultured CD34+ CD38- c-kit(low/-) cells initiated from CD34+ CD38- c-kit(low/-) cells remained dormant until 36 hr and entered cell cycle within 90 hr. Anti-TGF-beta increased the percentage of S/G2M phase postcultured CD34+ CD38- c-kit(high) cells (from 19.08 +/- 11.95 to 47.04 +/- 2.93%), but no significant change was observed in postcultured CD34+ CD38- c-kit(low/-) cells. These results suggest that endogenous TGF-beta plays an important role in the cell cycle arrest of c-kit(high) but not c-kit(low/-) cells in CD34+ CD38- cells, which proliferate without undergoing differentiation. The different regulatory mechanism of cell cycle entry of the CD34+ CD38- c-kit(high) and CD34+ CD38- c-kit(low/-) subsets might be the result of differences in their sensitivity to endogenous TGF-beta.
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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/ADP-ribosyl Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD34,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD38,
http://linkedlifedata.com/resource/pubmed/chemical/CD38 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Serum-Free,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Hematopoietic Cell Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-kit,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0902-4441
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
71
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
351-8
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:14667198-ADP-ribosyl Cyclase,
pubmed-meshheading:14667198-Adult,
pubmed-meshheading:14667198-Antigens, CD,
pubmed-meshheading:14667198-Antigens, CD34,
pubmed-meshheading:14667198-Antigens, CD38,
pubmed-meshheading:14667198-Bone Marrow Cells,
pubmed-meshheading:14667198-Cell Cycle,
pubmed-meshheading:14667198-Cell Differentiation,
pubmed-meshheading:14667198-Cell Division,
pubmed-meshheading:14667198-Cells, Cultured,
pubmed-meshheading:14667198-Culture Media, Serum-Free,
pubmed-meshheading:14667198-Cytokines,
pubmed-meshheading:14667198-Gene Expression Regulation,
pubmed-meshheading:14667198-Hematopoietic Cell Growth Factors,
pubmed-meshheading:14667198-Hematopoietic Stem Cells,
pubmed-meshheading:14667198-Humans,
pubmed-meshheading:14667198-Membrane Glycoproteins,
pubmed-meshheading:14667198-Proto-Oncogene Proteins c-kit,
pubmed-meshheading:14667198-Transforming Growth Factor beta
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pubmed:year |
2003
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pubmed:articleTitle |
Correlation of c-kit expression and cell cycle regulation by transforming growth factor-beta in CD34+ CD38- human bone marrow cells.
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pubmed:affiliation |
Department of Pediatrics, Hyogo College of Medicine 1-1 Mukogawa-cho, Nishinomiya, Hyogo, Japan. mori-ped@hyo-med.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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