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rdf:type |
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lifeskim:mentions |
umls-concept:C0007303,
umls-concept:C0019800,
umls-concept:C0029408,
umls-concept:C0208973,
umls-concept:C0392756,
umls-concept:C0598996,
umls-concept:C1333909,
umls-concept:C1516377,
umls-concept:C1517892,
umls-concept:C1517945,
umls-concept:C1704666
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pubmed:issue |
4
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pubmed:dateCreated |
2009-1-28
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pubmed:abstractText |
Osteoarthritis (OA) is the most common joint disease and typically begins with an aging-related disruption of the articular cartilage surface. Mechanisms leading to the aging-related cartilage surface degeneration remain to be determined. Here, we demonstrate that nonhistone chromatin protein high-mobility group box (HMGB) protein 2 is uniquely expressed in the superficial zone (SZ) of human articular cartilage. In human and murine cartilage, there is an aging-related loss of HMGB2 expression, ultimately leading to its complete absence. Mice genetically deficient in HMGB2 (Hmgb2(-/-)) show earlier onset of and more severe OA. This is associated with a profound reduction in cartilage cellularity attributable to increased cell death. These cellular changes precede glycosaminoglycan depletion and progressive cartilage erosions. Chondrocytes from Hmgb2(-/-) mice are more susceptible to apoptosis induction in vitro. In conclusion, HMGB2 is a transcriptional regulator specifically expressed in the SZ of human articular cartilage and supports chondrocyte survival. Aging is associated with a loss of HMGB2 expression and reduced cellularity, and this contributes to the development of OA.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-10391216,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-10490593,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-10558853,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-10741968,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-11262228,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-11465715,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-12027537,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-12127837,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-12672494,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-12687539,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-12759333,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-13130470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-14471899,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-14558093,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-14644851,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-14744997,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-14762107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-14871457,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-15146422,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-15334469,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-15374498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-15564063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-15719068,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-15727891,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-15800624,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-16626979,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-16912416,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-17384639,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-17468016,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-17548469,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-18054255,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-18383360,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-1841605,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-2325444,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-3632732,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-8441138,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-8890171,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-9671457,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19139395-9920774
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1091-6490
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
27
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pubmed:volume |
106
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1181-6
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:19139395-Aging,
pubmed-meshheading:19139395-Animals,
pubmed-meshheading:19139395-Apoptosis,
pubmed-meshheading:19139395-Cartilage, Articular,
pubmed-meshheading:19139395-Cell Survival,
pubmed-meshheading:19139395-Chromatin,
pubmed-meshheading:19139395-Gene Expression Regulation,
pubmed-meshheading:19139395-HMGB2 Protein,
pubmed-meshheading:19139395-Humans,
pubmed-meshheading:19139395-Joints,
pubmed-meshheading:19139395-Matrix Metalloproteinases,
pubmed-meshheading:19139395-Mice,
pubmed-meshheading:19139395-Osteoarthritis,
pubmed-meshheading:19139395-Protein Transport,
pubmed-meshheading:19139395-Proteoglycans
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pubmed:year |
2009
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pubmed:articleTitle |
Aging-related loss of the chromatin protein HMGB2 in articular cartilage is linked to reduced cellularity and osteoarthritis.
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pubmed:affiliation |
Division of Arthritis Research, The Scripps Research Institute, La Jolla, CA 92037, USA.
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pubmed:publicationType |
Journal Article
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