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Pathogenesis of rheumatoid arthritis: Insights into mechanisms of synovial hyperplasia and of reactive nitrogen species mediated inflammatory damage.

By Jan. Brun

Abstract

Synovial hyperplasia is a hallmark of rheumatoid arthritis (RA). This pathological change may be due to an increase in cell proliferation and/or a decrease in cell death (apoptosis). However, the rates at which these opposing mechanisms occur in the arthritic and control synovium, remain a subject of debate. Our objective was to address this debate using recently developed polyclonal antibodies to thymidylate synthase (TS, another potential cell proliferation marker), and activated caspase 3 and cleaved polyADPribose polymerase (PARP p85), two markers of apoptosis. PCNA and Ki-67, two well characterized proliferation markers were also used in this study. Germinal centers of human tonsil tissue were used as positive controls for proliferation and apoptosis. Another equally important factor in RA is the role of reactive nitrogen and oxygen species (RNOS) such as nitric oxide (NO) and superoxide (O 2-) in inflammation mediated protein damage. Such damage is evidenced by the immunohistochemical detection of nitrotyrosine in a variety of animal models and human inflammatory disorders. Therefore, I studied arthritic joint tissue for the presence of protein nitrotyrosine using immunohistochemical and immunoblotting techniques. (Abstract shortened by UMI.

Topics: Health Sciences, Pathology.
Publisher: University of Ottawa (Canada)
Year: 2001
OAI identifier: oai:www.ruor.uottawa.ca:10393/9422
Provided by: Recherche uO Research
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