DNA polymerase activity of cultured rheumatoid synovial cells

Spruance, Spotswood L.; Richards, Oliver C.; Smith, Charles B.; Ward, John

doi:10.1002/art.1780180306

Cited by 9 publications

(2 citation statements)

References 28 publications

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“…However. Spruance, Richards, Ward, and Smith (1974) showed reverse transcriptase activity in cultured rheumatoid synovial cell strains and also found it in normal synovial cell strains.…”

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confidence: 79%

DNA polymerase activity in rheumatoid synovial membranes.

Norval¹,

Ogilvie²,

Marmion³

1975

Annals of the Rheumatic Diseases

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Norval, M., Ogilvie, M. M., and Marmion, B. P. (1975). Annals ofthe Rheumatic Diseases, 34,[205][206][207][208][209][210][211][212]. DNA polymerase activity in rheumatoid synovial membranes. RNase-sensitive DNA polymerase activity was demonstrated in synovial membrane preparations from 23 out of 25 rheumatoid arthritis patients. Control groups consisted of twelve patients with osteoarthrosis, four with secondary osteoarthrosis, and twelve with other conditions. The last group showed no activity, while the results with the other two groups were varied. The properties of the polymerase enzyme, such as its stimulation by synthetic templates and inhibition by actinomycin D, were not consistent with it being associated with an oncogenicvirus; it seems to bemorelike that found in stimulated normal human lymphocytes, described as an RNA-primed DNA-directed DNA polymerase.

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“…However. Spruance, Richards, Ward, and Smith (1974) showed reverse transcriptase activity in cultured rheumatoid synovial cell strains and also found it in normal synovial cell strains.…”

mentioning

confidence: 79%

DNA polymerase activity in rheumatoid synovial membranes.

Norval¹,

Ogilvie²,

Marmion³

1975

Annals of the Rheumatic Diseases

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“…In analogous studies RA extracts of synovial membranes on the one hand, or cultured or cocultivated synovial cells on the other, were not shown to contain viral polymerases (Spruance et al, 1975;Norval et al, 1975). Less attention has been paid in studies of RA to the possible involvement of retrovirus with cells of the immune and immunoregulatory system.…”

mentioning

confidence: 99%

Viruses and lymphocytes in rheumatoid arthritis. II. Examination of lymphocytes and sera from patients with rheumatoid arthritis for evidence of retrovirus infection.

Hart¹,

McCormick²,

Marmion³

1979

Annals of the Rheumatic Diseases

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summARY The possible involvement of retroviruses in the aetiology of rheumatoid arthritis (RA) was investigated. Retrovirus antigens were not expressed on rheumatoid synovial and peripheral blood lymphocytes as judged by membrane immunofluorescence, radioimmunoassay, and complement-mediated cytotoxicity. The specific antiretroviral (anti-RD-144 and anti-SSAV) sera used in this study were produced in rabbits immunised with viral antigens grown in a homologous system (rabbit cells and medium supplemented with normal rabbit serum), avoiding non-specific immunofluorescence previously detected with donated antiretroviral sera. Immune complexes lodged in the rheumatoid synovial membranes did not contain, and other cells within the membranes did not express, retroviral antigens. Antibodies cross-reacting with primate retrovirus antigens were sought in sera from patients with 'autoimmune' diseases by means of solid phase radioimmunoassay. There were no retrovirus antibodies in the 3 groups of patients studied, that is, those with rheumatoid arthritis, systemic lupus erythematosus, and with non-RA conditions. Absorption of rheumatoid factor did not alter this conclusion. These results give little support to the hypothesis that activation of endogenous human retroviruses or an infection with horizontally transmitted retroviruses is associated with the rheumatoid process.

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The growth kinetics of synovial fibroblastic cells from inflammatory and noninflammatory arthropathies

Anastassiades

Ley

Wood

et al. 1978

Arthritis & Rheumatism

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The growth kinetics of subcultured human synovial fibroblasts from 16 patients with inflammatory and noninflammatory arthropathies were studied in antibiotic free media. The experimental design allowed a clear distinction between the growth rates and final saturation densities achieved. The effects of refeeding and of the serum concentration were evaluated for each line. Inflammatory lines achieved significantly higher final saturation densities and growth rates than noninflammatory lines for most protocols, but the differences between rheumatoid and nonrheumatoid groups were less marked. Inflammatory fibroblasts demonstrated a greater independence to nutritional and growth stimulatory factors in their microenvironment than noninflammatory fibroblasts.The modulation of fibroblastic proliferation in culture is under complex control, and many of the factors involved are incompletely understood (1). Nevertheless, untransformed fibroblastic cells often exhibit greater or lesser degrees of density-dependent inhibition of growth (DDI). One measurement of DDI is reflected by the final cell saturation density (FSD) achieved by the fibroblastic cells under defined conditions of refeeding the cultures and of serum supplementation (2,3).The precise mechanisms involved in DDI are uncertain, but one possibility is that it is effected by the actual contact between cells. A mechanism for this contact inhibition of growth based on mutual modification of surface carbohydrate moieties by surface glycosyltransferases (4) has received both considerable support (5,6) and criticism (7,8).However, the FSD achieved by fibroblastic cells can be affected by different sets of circumstances in the microenvironment of the culture other than those affecting the growth rate of the cells. For example, the authors had previously demonstrated that although a change in culture pH of human skin fibroblasts does not affect growth rates, the FSD at the higher pH values was always greater than that achieved at lower pH at any serum concentration between 1% and 20% (9). Nutritional effects, operative mainly through diffusion gradients of the larger molecules in the extracellular microenvironment (3,10), may also modulate DDI under certain circumstances. However, we have demonstrated that such diffusion effects cannot entirely account for the phenomenon of DDI under various conditions of nutrient availability and serum supplementation (10).Previously published work on the growth of human rheumatoid and nonrheumatoid synovial cells in

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DNA polymerase activity of cultured rheumatoid synovial cells

Cited by 9 publications

References 28 publications

DNA polymerase activity in rheumatoid synovial membranes.

DNA polymerase activity in rheumatoid synovial membranes.

Viruses and lymphocytes in rheumatoid arthritis. II. Examination of lymphocytes and sera from patients with rheumatoid arthritis for evidence of retrovirus infection.

The growth kinetics of synovial fibroblastic cells from inflammatory and noninflammatory arthropathies

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