Open AccessIndependent effects of interleukin‐1 on proteoglycan breakdown, proteoglycan synthesis, and prostaglandin E 2 release from cartilage in organ culture
Author(s) -
Arner Elizabeth C.,
Pratta Michael A.
Publication year - 1989
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/anr.1780320310
Subject(s) - proteoglycan , cartilage , chemistry , prostaglandin e2 , prostaglandin e , organ culture , stimulation , endocrinology , interleukin , medicine , pharmacology , microbiology and biotechnology , biochemistry , cytokine , biology , in vitro , anatomy
Abstract Exposure of bovine nasal cartilage in culture to interleukin‐1 (IL‐1) leads to a time‐ and concentration‐dependent stimulation of proteoglycan breakdown and prostaglandin E 2 (PGE 2 ) release, and to inhibition of proteoglycan synthesis. The threshold levels of IL‐1 required for initiating these effects were different, and IL‐1 was 10 times more potent in inhibiting synthesis than in stimulating breakdown of proteoglycan. Kinetic studies indicated that the effects on proteoglycan metabolism occurred earlier (16–24 hours) than those for PGE 2 release (48 hours). Selective effects were observed with inhibitors. Nonsteroidal antiinflammatory drugs blocked PGE 2 production in response to IL‐1, but had no effect on proteoglycan metabolism, and the antiarthritic drugs that blocked IL‐1–stimulated breakdown augmented the inhibition of proteoglycan synthesis. We suggest that the effects of IL‐1 on proteoglycan breakdown, proteoglycan synthesis, and PGE 2 release are mediated by independent post‐receptor mechanisms.