| pubmed-article:8200968 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8200968 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8200968 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
| pubmed-article:8200968 | lifeskim:mentions | umls-concept:C0596233 | lld:lifeskim |
| pubmed-article:8200968 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:8200968 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:8200968 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:8200968 | pubmed:dateCreated | 1994-7-7 | lld:pubmed |
| pubmed-article:8200968 | pubmed:abstractText | Interleukin-6 (IL-6) is a multifunctional cytokine which is made by osteoblasts and has diverse effects on bone metabolism. We studied the interaction of IL-6 with the Ca2+ and cAMP signaling systems in the osteoblastic cell line UMR-106 and in primary osteoblastic cultures derived from neonatal rat calvariae. IL-6 did not alter basal intracellular calcium concentration ([Ca2+]i) but inhibited Ca2+ transients induced by parathyroid hormone (PTH), prostaglandin E2 (PGE2), and endothelin-1 in both dose- (100-400 U/ml) and time- (4-48 h) dependent manners. The effect of the cytokine was abolished by the tyrosine kinase inhibitor, herbimycin A (50 ng/ml). The IL-6 effect on the Ca2+ message system was related to suppressed production of hormonally induced inositol 1,4,5-triphosphate and inhibition of Ca2+ release from intracellular stores. Hormonally induced calcium entry pathways (estimated by using Mn2+ as a surrogate for Ca2+) were not, however, altered by the cytokine. IL-6 did not modulate cAMP generation in osteoblasts. With respect to osteoblast function, IL-6, although having no effect on cell proliferation by itself, greatly enhanced the antiproliferative effect of PGE2 and PTH. Because the production of IL-6 in osteoblasts is stimulated by calciotropic hormones (e.g., PTH and PGE2), the suppressive effect of the cytokine on hormonally induced Ca2+ transients may serve as an autocrine/paracrine mechanism for modulating the effect of hormones on bone metabolism. | lld:pubmed |
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| pubmed-article:8200968 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8200968 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8200968 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:8200968 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8200968 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:8200968 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:8200968 | pubmed:author | pubmed-author:KleemanC RCR | lld:pubmed |
| pubmed-article:8200968 | pubmed:author | pubmed-author:GreenJJ | lld:pubmed |
| pubmed-article:8200968 | pubmed:author | pubmed-author:SchotlandSS | lld:pubmed |
| pubmed-article:8200968 | pubmed:author | pubmed-author:SellaZZ | lld:pubmed |
| pubmed-article:8200968 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8200968 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:8200968 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8200968 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8200968 | pubmed:pagination | 2340-50 | lld:pubmed |
| pubmed-article:8200968 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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