Ra. Jacobs et al., RHEUMATOID SYNOVIAL CELL-PROLIFERATION, TRANSFORMATION AND FIBRONECTIN SECRETION IN CULTURE, Clinical and experimental rheumatology, 13(6), 1995, pp. 717-723
Objective. There is some experimental evidence that patients with rheu
matoid arthritis (RA) have a defect in the control of cellular prolife
ration. To examine this further, synovial cells from patients with RA
and osteoarthritis controls (OA) were studied for phenotypic character
istics of transformation and proliferation. Methods. Synovial cells gr
own in vitro were studied to determine the extent of proliferation, an
chorage-independent growth, growth under reduced serum conditions, fib
ronectin secretion, and the presence of cell proliferation antigens.Re
sults. RA synovial cell proliferation was less than that recorded for
normal skin fibroblasts and was not increased compared to OA synovial
cells. Studies of growth in soft agarose showed no colony formation by
RA or OA synovial cells after 28 days, indicating that anchorage-inde
pendent growth does not occur. At low serum concentrations RA and OA s
ynovial cells showed similar growth. Fibronectin was constant for each
cell line studied irrespective of the cell number or diagnosis. RA ce
lls did not show an increased rate of fibronectin secretion. RA cells
did not show art increased expression of proliferating cell antigens.
Conclusion. These studies do not support the concept that defective pr
oliferation of synovial cells is a major factor in the pathogenesis of
RA.