Effects of murine recombinant interleukin 1 on intact homologous articular cartilage: a quantitative and autoradiographic study.

Effect of interleukin 17 on proteoglycan degradation in murine knee joints

“…As reported for IL1, depletion of proteoglycan seems to result from a local action of IL17 on cartilage as joint inflammation and cell recruitment are very mild 17. On the contrary, and unlike IL1β, where prolonged suppression of proteoglycan synthesis appears as a key factor,20 our data indicate that IL17 induces proteoglycan loss primarily through increased degradation without a detectable change in biosynthesis rate.…”

Reduction of interleukin‐17–induced inhibition of chondrocyte proteoglycan synthesis in intact murine articular cartilage by interleukin‐4

“…We have previously shown that IL-1 induces a dose-dependent inhibition of chondrocyte PG synthesis in intact murine articular cartilage (34). In the present study, preincubation with IL-4 dose-dependently sup- pressed the IL-1-induced inhibition of chondrocyte PG synthesis (Table 2).…”

Inflammation-mediated chondrocyte unresponsiveness to insulin-like growth factor-1 is not caused by H2O2

“…In addition, we found that H202 was not able to damage the lGF-i receptor, as measured by 125I-IGF-1 binding. H202 could induce inhibition ofchondrocyte PG synthesis [1], but this inhibition must be related to a mechanism other than disturbance of IGF-1 signaling. This is in line with the recent study of Baker & Lowther [7], who have shown that the inhibition of chondrocyte PG synthesis due to HzO 2 exposure is caused by an inactivation of glyceraldehyde-3-phosphatedehydrogenase.…”

“…The phenomenon of inhibition of chondrocyte proteoglycan (PG) synthesis during an experimental arthritis could be provoked by suppressive mediators such as IL-1 or hydrogen-peroxide [1,2]. On the other hand, inhibition of PG synthesis could be looked upon as the result of lack of anabolic stimuli.…”