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- W76786315 abstract "Research Article1 January 1992free access Expression of prepro-enkephalin in human articular chondrocytes is linked to cell proliferation. P.M. Villiger P.M. Villiger Sam and Rose Stein Institute for Research on Aging, Department of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author M. Lotz M. Lotz Sam and Rose Stein Institute for Research on Aging, Department of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author P.M. Villiger P.M. Villiger Sam and Rose Stein Institute for Research on Aging, Department of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author M. Lotz M. Lotz Sam and Rose Stein Institute for Research on Aging, Department of Medicine, University of California, San Diego, La Jolla 92093. Search for more papers by this author Author Information P.M. Villiger1 and M. Lotz1 1Sam and Rose Stein Institute for Research on Aging, Department of Medicine, University of California, San Diego, La Jolla 92093. The EMBO Journal (1992)11:135-143https://doi.org/10.1002/j.1460-2075.1992.tb05036.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info This study shows that cultured human articular chondrocytes express high levels of 1.4 kb prepro-enkephalin mRNA. Chondrocytes store met-enkephalin intracellularly and secrete this neuropeptide in mature as well as in precursor form. Gene expression is inducible by serum factors. High levels of prepro-enkephalin mRNA are detected in proliferating chondrocytes but not in confluent, contact-inhibited cells. Phorbol myristate acetate and dibutyryl cyclic AMP, but not dexamethasone, increase levels of prepro-enkephalin mRNA. Furthermore, transforming growth factor beta (TGF beta) and platelet derived growth factor (PDGF) upregulate gene expression, whereas retinoic acid, which inhibits chondrocyte proliferation, suppresses both basal and induced gene expression. Using in situ hybridization it is shown that only 1–3% of primary chondrocytes express prepro-enkephalin mRNA, whereas 52 +/− 12% of subcultured cells are strongly positive. Analysis of DNA synthesis, by autoradiography of incorporated [3H]thymidine, shows that these numbers correspond to the percentage of cells in S-phase of the cell cycle. In cultures of primary chondrocytes TGF beta promotes the formation of cartilage nodules and stimulates proliferation of adherent cells. This is associated with high levels of prepro-enkephalin mRNA in proliferating cells but not in contact-inhibited cells in cartilage nodules. In contrast, formation of cartilage nodules, proliferation and the expression of enkephalin are suppressed by interleukin-1 beta. In summary, expression of prepro-enkephalin in human articular chondrocytes is differentially controlled by cartilage regulatory factors and closely associated with cell proliferation. Previous ArticleNext Article Volume 11Issue 11 January 1992In this issue RelatedDetailsLoading ..." @default.
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- W76786315 title "Expression of prepro-enkephalin in human articular chondrocytes is linked to cell proliferation." @default.
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