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Digitale Medien

Interleukin-1β and interleukin-1α stimulate the N-acetyl-β-glucosaminidase activity of human synovial cells (1987)

Clarris, B. J. ; Fraser, J. R. E. ; Ash, P. ; [weitere]

Springer

Rheumatology international 7 (1987), S. 271-275

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ISSN: 1437-160X

Schlagwort(e): Synovial cells ; N-acetyl-β-glucosaminidase ; Interleukin-1 ; Synovial activator ; Rheumatoid arthritis

Quelle: Springer Online Journal Archives 1860-2000

Thema: Medizin

Notizen: Summary The properties of synovial cells are altered in vitro by monocyte-macrophage polypeptides (monokines), and these changes could explain some of the properties of the inflamed synovium in rheumatoid disease. Purified monokines have become available only recently for testing on the target synovial cells. We report here that purified human interleukin (IL)-1β and recombinant human Il-1α stimulate the extracellular activity of the lysosomal hydrolase, N-acetyl-β-glucosaminidase (NAG), of human synovial fibroblast-like cells. In contrast, another monokine, synovial activator, does not increase the NAG activity. Thus NAG is another cellular activity which can be modulated by interleukin-1.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00270528

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Digitale Medien

Peripheral blood mononuclear cells stimulate N-acetyl-β-glucosaminidase levels of human synovial fibroblast-like cells (1985)

Clarris, B. J. ; Hamilton, J. A.

Springer

Rheumatology international 5 (1985), S. 55-60

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ISSN: 1437-160X

Schlagwort(e): Synovial cells ; Lysosomes ; N-acetyl-β-glucosaminidase ; Prostaglandins ; Rheumatoid arthritis

Quelle: Springer Online Journal Archives 1860-2000

Thema: Medizin

Notizen: Summary Fibroblast-like synovial cells isolated from intact joints of non-arthritic human donors released up to nine-times higher activity of the lysosomal acid hydrolase N-acetyl-β-glucosaminidase (NAG) than controls when incubated in conditioned medium from homologous peripheral blood mononuclear cells (MCCM). This increase occurred without decrease in cell numbers or other evidence of cytotoxicity. An increase in cell-associated NAG activity was also suggested, but this was not statistically significant. Indomethacin present during production of MCCM or added with MCCM to fibroblast cultures did not alter the response to MCCM, indicating that the effect of MCCM was not due to the presence of products from the cyclo-oxygenase pathway. At a concentration known to block protein synthesis in most cells (10−5 M), cycloheximide markedly suppressed the NAG releasing response to MCCM. The secretion of NAG due to MCCM was not affected by all-trans retinoic acid (10−6 M) but was suppressed by the corticosteroid, dexamethasone.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00270297

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