Literature DB >> 10403282

Apoptotic chondrocyte death in rheumatoid arthritis.

H A Kim1, Y W Song.   

Abstract

OBJECTIVE: Recently, chondrocytes were shown to undergo apoptosis by the addition of nitric oxide and by coupling of Fas/Fas ligand in vitro, suggesting the possibility that chondrocytes have an inherent programmed cell death pathway that operates in adult cartilage. Chondrocyte apoptosis was verified in situ in articular cartilage samples from humans with osteoarthritis (OA) and from an animal model of OA. The present study investigates apoptotic chondrocyte death and the expression of Bcl-2 and Fas in rheumatoid arthritis (RA) cartilage.
METHODS: Cartilage samples were obtained from 13 RA patients at the time of joint replacement surgery and from 8 normal subjects at autopsy. Apoptotic chondrocytes were observed and counted in hematoxylin and eosin-stained cartilage specimens. Apoptosis was verified by TUNEL, electron microscopy, and DNA ladder assay. Bcl-2 and Fas expression were evaluated by immunohistochemistry.
RESULTS: Apoptotic cells were frequently observed in RA cartilage, whereas normal cartilage rarely showed apoptotic cells (3.01% versus 0.15%, respectively), a finding that was further confirmed by TUNEL staining. On electron microscopy, numerous apoptotic cells with typical chromatin condensation were observed in RA cartilage. DNA from RA cartilage also revealed 180-basepair nucleosome ladders on electrophoresis. Bcl-2 expression was significantly lower in RA cartilage than in normal cartilage (23.3% versus 43.1%, respectively), whereas Fas expression was not statistically different.
CONCLUSION: Apoptotic chondrocyte death and decreased Bcl-2 expression were verified in RA cartilage. They might provide a novel model system for the research of cartilage breakdown and joint destruction in RA.

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Year:  1999        PMID: 10403282     DOI: 10.1002/1529-0131(199907)42:7<1528::AID-ANR28>3.0.CO;2-9

Source DB:  PubMed          Journal:  Arthritis Rheum        ISSN: 0004-3591


  24 in total

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2.  Chondrocyte Apoptosis in Rheumatoid Arthritis: Is Preventive Therapy Possible?

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3.  Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis.

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4.  Interleukin-1beta induces death in chondrocyte-like ATDC5 cells through mitochondrial dysfunction and energy depletion in a reactive nitrogen and oxygen species-dependent manner.

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5.  Inflammatory synovial fluid microenvironment drives primary human chondrocytes to actively take part in inflammatory joint diseases.

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Authors:  R T Benson; S M McDonnell; H J Knowles; J L Rees; A J Carr; P A Hulley
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7.  Inhibition of NF-kappaB renders human juvenile costal chondrocyte cell lines sensitive to TNF-alpha-mediated cell death.

Authors:  Ho Sung Yoon; Hyun Ah Kim; Yeong Wook Song
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8.  Increased Bcl-2/p53 ratio in human osteoarthritic cartilage: a possible role in regulation of chondrocyte metabolism.

Authors:  F Iannone; C De Bari; C Scioscia; V Patella; G Lapadula
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Review 9.  Cellular FLICE-inhibitory protein: an attractive therapeutic target?

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10.  Prologation of c-Jun N-terminal kinase is associated with cell death induced by tumor necrosis factor alpha in human chondrocytes.

Authors:  Ho Sung Yoon; Hyun Ah Kim
Journal:  J Korean Med Sci       Date:  2004-08       Impact factor: 2.153

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