Source:http://linkedlifedata.com/resource/pubmed/id/21363931
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2011-4-22
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| pubmed:abstractText |
IL-33 is an important inflammatory mediator in allergy, asthma, and joint inflammation, acting via its receptor, ST2L, to elicit Th? cell cytokine secretion. IL-33 is related to IL-1 and IL-18, which both influence bone metabolism, IL-18 in particular inhibiting osteoclast formation and contributing to PTH bone anabolic actions. We found IL-33 immunostaining in osteoblasts in mouse bone and IL-33 mRNA expression in cultured calvarial osteoblasts, which was elevated by treatment with the bone anabolic factors oncostatin M and PTH. IL-33 treatment strongly inhibited osteoclast formation in bone marrow and spleen cell cultures but had no effect on osteoclast formation in receptor activator of nuclear factor-?B ligand/macrophage colony-stimulating factor-treated bone marrow macrophage (BMM) or RAW264.7 cultures, suggesting a lack of direct action on immature osteoclast progenitors. However, osteoclast formation from BMM was inhibited by IL-33 in the presence of osteoblasts, T cells, or mature macrophages, suggesting these cell types may mediate some actions of IL-33. In bone marrow cultures, IL-33 induced mRNA expression of granulocyte macrophage colony-stimulating factor, IL-4, IL-13, and IL-10; osteoclast inhibitory actions of IL-33 were rescued only by combined antibody ablation of these factors. In contrast to osteoclasts, IL-33 promoted matrix mineral deposition by long-term ascorbate treated primary osteoblasts and reduced sclerostin mRNA levels in such cultures after 6 and 24 h of treatment; sclerostin mRNA was also suppressed in IL-33-treated calvarial organ cultures. In summary, IL-33 stimulates osteoblastic function in vitro but inhibits osteoclast formation through at least three separate mechanisms. Autocrine and paracrine actions of osteoblast IL-33 may thus influence bone metabolism.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1945-7170
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
152
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1911-22
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| pubmed:meshHeading |
pubmed-meshheading:21363931-Animals,
pubmed-meshheading:21363931-Animals, Newborn,
pubmed-meshheading:21363931-Bone Marrow Cells,
pubmed-meshheading:21363931-Calcification, Physiologic,
pubmed-meshheading:21363931-Cell Differentiation,
pubmed-meshheading:21363931-Cell Line,
pubmed-meshheading:21363931-Cells, Cultured,
pubmed-meshheading:21363931-Dendritic Cells,
pubmed-meshheading:21363931-Extracellular Matrix,
pubmed-meshheading:21363931-Gene Expression,
pubmed-meshheading:21363931-Humans,
pubmed-meshheading:21363931-Immunohistochemistry,
pubmed-meshheading:21363931-Interleukin-13,
pubmed-meshheading:21363931-Macrophages,
pubmed-meshheading:21363931-Mice,
pubmed-meshheading:21363931-Mice, Inbred C57BL,
pubmed-meshheading:21363931-Mice, Knockout,
pubmed-meshheading:21363931-Oncostatin M,
pubmed-meshheading:21363931-Osteoblasts,
pubmed-meshheading:21363931-Osteoclasts,
pubmed-meshheading:21363931-Parathyroid Hormone,
pubmed-meshheading:21363931-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21363931-Spleen,
pubmed-meshheading:21363931-T-Lymphocytes
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| pubmed:year |
2011
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| pubmed:articleTitle |
Interleukin-33, a target of parathyroid hormone and oncostatin m, increases osteoblastic matrix mineral deposition and inhibits osteoclast formation in vitro.
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| pubmed:affiliation |
Prince Henry's Institute, Monash Medical Centre, Clayton Road, Clayton, Victoria 3168, Australia.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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