AI Article Synopsis
- Recombinant human interleukin-1 alpha and beta (rhIL-1 alpha/beta) promote the release of glycosaminoglycan (GAG) from bovine nasal cartilage in a time- and concentration-dependent manner, with rhIL-1 alpha being more effective.
- Maximum GAG release occurs between six to eight days of exposure, while both cytokines also inhibit the synthesis of GAG.
- The presence of rhIL-1 has no effect on dead cartilage, and specific inhibitors can reduce the cartilage matrix resorption stimulated by these interleukins.
Article Abstract
Recombinant human interleukin-1 alpha (rhIL-1 alpha) and recombinant human interleukin 1 beta (rhIL-1 beta) stimulated the time- and concentration-dependent release of glycosaminoglycan (GAG) from bovine nasal cartilage explants. Maximum GAG release occurred during six to eight days of cartilage exposure to either species of rhIL-1; and rhIL-1 alpha was consistently more potent than rhIL-1 beta. In addition to inducing cartilage matrix resorption, rhIL-1 alpha and rhIL-1 beta also inhibited the incorporation of [35SO4]sulfate into cartilage, which is a reflection of the suppression of GAG synthesis. IL-1 had no capacity to stimulate GAG relase from or inhibit GAG synthesis by dead cartilage. Cycloheximide, an inhibitor of protein synthesis, and 1, 10-phenanthroline, a metalloproteinase inhibitor, suppressed rhIL-1-stimulated cartilage matrix resorption. Polyclonal antisera to rhIL-1 alpha and rhIL-1 beta specifically neutralized the respective cytokines.
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| http://dx.doi.org/10.1007/BF00914921 | DOI Listing |
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