Source:http://linkedlifedata.com/resource/pubmed/id/21353395
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
umls-concept:C0001811,
umls-concept:C0004083,
umls-concept:C0007303,
umls-concept:C0017262,
umls-concept:C0026809,
umls-concept:C0086597,
umls-concept:C0108685,
umls-concept:C0185117,
umls-concept:C0225369,
umls-concept:C0231337,
umls-concept:C0249197,
umls-concept:C0288472,
umls-concept:C1333655,
umls-concept:C1420626,
umls-concept:C2911684
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| pubmed:issue |
4
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| pubmed:dateCreated |
2011-4-25
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| pubmed:abstractText |
Growth arrest and DNA damage-inducible protein 45? (GADD45?) is expressed in normal and early osteoarthritic articular cartilage. We recently reported that GADD45? enhances CCAAT/enhancer binding protein ? (C/EBP?) activation in vitro. This study was undertaken in order to determine whether GADD45? is expressed with C/EBP? in aging articular cartilage. We also investigated whether the synergistic expression of GADD45? and C/EBP? may be involved in the mechanism of chondrocyte senescence. Senescence-accelerated mice (SAMP1) were used as a model of aging. GADD45?, C/EBP?, and p21 were analyzed by immunohistochemistry. A luciferase reporter assay using ATDC5 cells was performed in order to examine p21 as a target gene of the GADD45?/C/EBP? cascade. GADD45? exhibited increased expression in the aging articular cartilage of SAMP1 mice compared to that in control mice. The co-localization of GADD45? and C/EBP? was confirmed by double immunostaining. The synergistic mechanisms of GADD45? and C/EBP? on the gene regulation of p21, a molecule related to cellular senescence, were verified by a p21-luciferase reporter assay. Co-expression of C/EBP? and p21 was confirmed. These observations suggest that the synergism between GADD45? and C/EBP? may play an important role in cellular senescence in the aging articular cartilage.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/CCAAT-Enhancer-Binding Protein-beta,
http://linkedlifedata.com/resource/pubmed/chemical/Gadd45b protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/p21-Activated Kinases
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
1618-0631
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| pubmed:author | |
| pubmed:copyrightInfo |
Crown Copyright © 2011. Published by Elsevier GmbH. All rights reserved.
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| pubmed:issnType |
Electronic
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| pubmed:day |
15
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| pubmed:volume |
207
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
225-31
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| pubmed:meshHeading |
pubmed-meshheading:21353395-Aging,
pubmed-meshheading:21353395-Animals,
pubmed-meshheading:21353395-Antigens, Differentiation,
pubmed-meshheading:21353395-CCAAT-Enhancer-Binding Protein-beta,
pubmed-meshheading:21353395-Cartilage, Articular,
pubmed-meshheading:21353395-Cell Aging,
pubmed-meshheading:21353395-Cell Line,
pubmed-meshheading:21353395-Chondrocytes,
pubmed-meshheading:21353395-DNA Damage,
pubmed-meshheading:21353395-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:21353395-Luciferases,
pubmed-meshheading:21353395-Male,
pubmed-meshheading:21353395-Mice,
pubmed-meshheading:21353395-Mice, Inbred C57BL,
pubmed-meshheading:21353395-Mice, Transgenic,
pubmed-meshheading:21353395-Models, Animal,
pubmed-meshheading:21353395-Osteoarthritis,
pubmed-meshheading:21353395-Promoter Regions, Genetic,
pubmed-meshheading:21353395-Signal Transduction,
pubmed-meshheading:21353395-p21-Activated Kinases
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| pubmed:year |
2011
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| pubmed:articleTitle |
Senescence of chondrocytes in aging articular cartilage: GADD45? mediates p21 expression in association with C/EBP? in senescence-accelerated mice.
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| pubmed:affiliation |
Orthopaedic Surgery, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1, Sakuragaoka, Kagoshima, 890-8520, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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