Expression of IL-1 genes in human and bovine chondrocytes: a mechanism for autocrine control of cartilage matrix degradation.
In this report we describe the presence of interleukin-1 activity in medium conditioned by bovine articular cartilage. Preparations partially purified by Sephacryl S200 chromatography (Mr 18000-25000) stimulate murine thymocyte proliferation in the lymphocyte activation factor assay. Furthermore, the factor(s) activate cartilage tissue to secrete a protease which is essential for the activity of purified synovial collagenase. We also demonstrate the presence of mRNA coding for IL-1 alpha and beta in human articular chondrocytes and conclude that the human monocytic and chondrocytic mRNAs are identical. Our results demonstrating cartilage expression of IL-1 genes suggest the possibility of an autocrine mechanism whereby chondrocyte production of matrix degrading proteases is initiated by chondrocyte derived IL-1.
D000328:Adult; D000818:Animals; D001681:Biological Assay; D002358:Cartilage, Articular / Q000378:metabolism*; D002417:Cattle; D004789:Enzyme Activation; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics*; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D003012:Microbial Collagenase / Q000378:metabolism; D008970:Molecular Weight; D012333:RNA, Messenger / Q000378:metabolism
D007375:Interleukin-1; D012333:RNA, Messenger; D003012:Microbial Collagenase