Advertisement
Research Article Free access | 10.1172/JCI116383
Department of Pathology, Jewish Hospital of St. Louis, Washington University, Missouri 63110.
Find articles by Lacey, D. in: JCI | PubMed | Google Scholar
Department of Pathology, Jewish Hospital of St. Louis, Washington University, Missouri 63110.
Find articles by Grosso, L. in: JCI | PubMed | Google Scholar
Department of Pathology, Jewish Hospital of St. Louis, Washington University, Missouri 63110.
Find articles by Moser, S. in: JCI | PubMed | Google Scholar
Department of Pathology, Jewish Hospital of St. Louis, Washington University, Missouri 63110.
Find articles by Erdmann, J. in: JCI | PubMed | Google Scholar
Department of Pathology, Jewish Hospital of St. Louis, Washington University, Missouri 63110.
Find articles by Tan, H. in: JCI | PubMed | Google Scholar
Department of Pathology, Jewish Hospital of St. Louis, Washington University, Missouri 63110.
Find articles by Pacifici, R. in: JCI | PubMed | Google Scholar
Department of Pathology, Jewish Hospital of St. Louis, Washington University, Missouri 63110.
Find articles by Villareal, D. in: JCI | PubMed | Google Scholar
Published April 1, 1993 - More info
IL-1-induced osteoblast IL-6 production represents one possible mechanism by which IL-1 augments bone resorption. In this report, we show that the murine osteoblastic cell line (MC3T3-E1) expresses type 1 IL-1 receptors based on 125I-HrIL1 alpha binding, blocked by type 1 IL-1R antibodies (35F5), and analysis of MC3T3 RNA by reverse transcription (RT)-DNA amplification and Northern analysis. MC3T3 cells do not express detectable type 2 IL-1R mRNA by RT-DNA amplification. IL-1 induces (IL-1 ED50, 0.1 pM) IL-6 production through the type 1 IL-1R as 35F5 antibodies block IL-1-stimulated IL-6 production. Vitamin D3 increases IL-1R expression dose- and metabolite-dependently, with 1,25-(OH)2D3 having the greatest potency, and also enhances IL-1's capacity to stimulate IL-6 production at low IL-1 levels. Both IL-1 and 1,25-(OH)2D3 induce type 1 IL-1R and not type 2 IL-1R upregulation based on ligand binding and RT-DNA amplification. Increased IL-1R expression requires a 5-7-h treatment and is protein/RNA synthesis dependent. These observations imply that IL-1-induced IL-6 production in osteoblasts is mediated by type 1 IL-1Rs and that increased IL-1R expression could play a role in mediating IL-1-induced skeletal responses.
Images.