B. Kurz et al., Articular chondrocytes and synoviocytes in a co-culture system: influence on reactive oxygen species-induced cytotoxicity and lipid peroxidation, CELL TIS RE, 296(3), 1999, pp. 555-563
Objective: A new co-culture system of rat articular chondrocytes and synovi
ocytes (HIG-82; cell line) was incubated with phorbol myristate acetate (PM
A), H2O2 or a combination of Fe2+ and ascorbic acid to simulate inflammatio
n-like radical attacks in articular joints. Methods: Chondrocytes were char
acterized by immunocytochemistry against collagen type II, transmission ele
ctron (TEM) and light microscopy. Lipid peroxidation was investigated by me
asuring thiobarbituric-acid-reactive material in the supernatants, cytotoxi
city by determining release of lactate dehydrogenase and proliferation by m
easuring [H-3]thymidine incorporation, culture protein and DNA. Results: PM
A or Fe2+ and ascorbic acid induced lipid peroxidation in chondrocytes and
synoviocytes that was decreased significantly in co-cultures. PMA and H2O2,
dose dependently induced release of lactate dehydrogenase in chondrocytes,
which was lowered in co-cultures or in previously co-cultured chondrocytes
to a nearly basal level. In contrast, conditioned media of synoviocyte cul
tures showed no lowering effect on the radical-induced toxicity. Protection
against H2O2-induced damage of cellular membranes by co-culturing was also
shown by TEM. Synoviocytes released chondrocyte-stimulating growth factors
spontaneously without previous interaction. Conclusion: Chondrocytes estab
lish protective mechanisms against reactive oxygen species via an interacti
on with synoviocytes. Our co-culture model presents a possible way to study
mechanisms of inflammation in articular joints under defined conditions.