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http://purl.uniprot.org/citations/12110441http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12110441http://www.w3.org/2000/01/rdf-schema#comment"Interleukin-11 (IL-11) is a stromal cell-derived cytokine that can enhance osteoclast formation and stimulate bone resorption. In the present study, the characteristics of the resorptive effect of IL-11 in mouse calvarial bones were investigated. Both recombinant mouse IL-11 and human IL-11 caused concentration- and time-dependent stimulations of (45)Ca release from prelabeled mouse calvariae. Half-maximal responses were obtained at 0.7 ng/mL (approximately 40 pmol/L). Mouse and human IL-11 also stimulated release of (3)H from [(3)H]-proline-labeled bones. The magnitude of the (45)Ca and (3)H release (1.4-1.6-fold) caused by a maximally effective concentration of IL-11 was less than the stimulation (2.5-4.0-fold) elicited by a maximum concentration of parathyroid hormone (PTH). Release of (45)Ca by IL-11 was unaffected by the mitotic inhibitors, hydroxyurea and aphidicolin. In addition to resorption of bone, IL-11 caused a small (1.5-2.0-fold) enhancement of prostaglandin E(2) (PGE(2)) biosynthesis in calvariae, but had no effect on the mRNA expression of cyclooxygenase-1 and -2, or cytosolic phospholipase A(2). Indomethacin and flurbiprofen abolished the formation of PGE(2) and partially reduced (45)Ca release stimulated by IL-11. When either mouse interleukin-4 (IL-4) or interleukin-13 (IL-13) was added to calvariae treated with IL-11, (45)Ca release was inhibited. Resorption caused by IL-11 was also inhibited by both anti-mouse glycoprotein 130 (gp130) and an antibody neutralizing IL-11, but these agents had no effect on (45)Ca release caused by PTH or 1,25(OH)(2)vitamin D(3) (D(3)). Real-time, quantitative polymerase chain reaction (PCR) analysis (TaqMan PCR) and semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) demonstrated that IL-11 caused concentration-dependent enhancements of receptor activator of nuclear factor-kappaB ligand (RANKL) and osteoprotegerin (OPG) mRNA, without affecting the mRNA expression of RANK. Mouse RANKL stimulated (45)Ca release in the calvarial bones. The stimulatory effects of RANKL and IL-11 were inhibited by mouse OPG. These data demonstrate that IL-11 stimulates osteoclastic resorption in mouse calvariae by mechanisms that are independent of cell proliferation; partially dependent on prostaglandin biosynthesis; sensitive to inhibition by IL-4, IL-13, and OPG; and associated with enhanced expression of RANKL and OPG. In addition, IL-11 was not found to play an essential role in resorption stimulated by other calciotropic agents in calvariae."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.org/dc/terms/identifier"doi:10.1016/s8756-3282(02)00784-6"xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/author"Andersson S."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/author"Roth C."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/author"Backman A."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/author"Lerner U.H."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/author"Ahlen J."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/author"Conaway H.H."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/author"Mukohyama H."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/date"2002"xsd:gYear
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/name"Bone"xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/pages"242-251"xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/title"Characterization of the bone-resorptive effect of interleukin-11 in cultured mouse calvarial bones."xsd:string
http://purl.uniprot.org/citations/12110441http://purl.uniprot.org/core/volume"31"xsd:string
http://purl.uniprot.org/citations/12110441http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/12110441
http://purl.uniprot.org/citations/12110441http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/12110441
http://purl.uniprot.org/uniprot/#_A3KPB8-mappedCitation-12110441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12110441
http://purl.uniprot.org/uniprot/#_F7A7F2-mappedCitation-12110441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12110441
http://purl.uniprot.org/uniprot/#_Q3V0U3-mappedCitation-12110441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12110441
http://purl.uniprot.org/uniprot/#_P47873-mappedCitation-12110441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12110441
http://purl.uniprot.org/uniprot/F7A7F2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/12110441
http://purl.uniprot.org/uniprot/Q3V0U3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/12110441
http://purl.uniprot.org/uniprot/A3KPB8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/12110441
http://purl.uniprot.org/uniprot/P47873http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/12110441
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