rdf:type |
|
lifeskim:mentions |
umls-concept:C0009336,
umls-concept:C0021755,
umls-concept:C0086418,
umls-concept:C0205161,
umls-concept:C0205217,
umls-concept:C0225369,
umls-concept:C0332437,
umls-concept:C0332453,
umls-concept:C0439849,
umls-concept:C0441889,
umls-concept:C0445223,
umls-concept:C1552599,
umls-concept:C1704787
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pubmed:issue |
11
|
pubmed:dateCreated |
2010-9-27
|
pubmed:abstractText |
Early osteoarthritis (OA) is poorly understood, but abnormal chondrocyte morphology might be important. We studied IL-1? and pericellular collagen type VI in morphologically normal and abnormal chondrocytes. In situ chondrocytes within explants from nondegenerate (grade 0/1) areas of human tibial plateaus (n = 21) were fluorescently labeled and visualized [2-photon laser scanning microscopy (2PLSM)]. Normal chondrocytes exhibited a "smooth" membrane surface, whereas abnormal cells were defined as demonstrating ?1 cytoplasmic process. Abnormal chondrocytes were further classified by number and average length of cytoplasmic processes/cell. IL-1? or collagen type VI associated with single chondrocytes were visualized by fluorescence immuno-histochemistry and confocal laser scanning microscopy (CLSM). Fluorescence was quantified as the number of positive voxels (i.e., 3D pixels with fluorescence above baseline)/cell. IL-1?-associated fluorescence increased between normal and all abnormal cells in the superficial (99.7 ± 29.8 [11 (72)] vs. 784 ± 382 [15 (132)]; p = 0.04, positive voxels/cell) and deep zones (66.5 ± 29.4 [9 (64)] vs. 795 ± 224 [9 (56)]; p = 0.006). There was a correlation (r(2)?= 0.988) between the number of processes/cell (0-5) and IL-1?, and an increase particularly with short processes (?5?µm; p = 0.022). Collagen type VI coverage and thickness decreased (p < 0.001 and p = 0.005, respectively) with development of processes. Abnormal chondrocytes in macroscopically nondegenerate cartilage demonstrated a marked increase in IL-1? and loss of pericellular type VI collagen, changes that could lead to cartilage degeneration.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20872589-10222218,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20872589-10229409,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/20872589-9627008
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1554-527X
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pubmed:author |
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pubmed:copyrightInfo |
© 2010 Orthopaedic Research Society.
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pubmed:issnType |
Electronic
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pubmed:volume |
28
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1507-14
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pubmed:dateRevised |
2011-8-25
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pubmed:meshHeading |
pubmed-meshheading:20872589-Aged,
pubmed-meshheading:20872589-Aged, 80 and over,
pubmed-meshheading:20872589-Chondrocytes,
pubmed-meshheading:20872589-Collagen Type VI,
pubmed-meshheading:20872589-Female,
pubmed-meshheading:20872589-Humans,
pubmed-meshheading:20872589-Interleukin-1beta,
pubmed-meshheading:20872589-Male,
pubmed-meshheading:20872589-Middle Aged,
pubmed-meshheading:20872589-Osteoarthritis
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pubmed:year |
2010
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pubmed:articleTitle |
Abnormal human chondrocyte morphology is related to increased levels of cell-associated IL-1? and disruption to pericellular collagen type VI.
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pubmed:affiliation |
Centre for Integrative Physiology, School of Biomedical Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, Scotland, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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