| pubmed-article:15845540 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0005953 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0162597 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0242184 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0919432 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:15845540 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:15845540 | pubmed:issue | 24 | lld:pubmed |
| pubmed-article:15845540 | pubmed:dateCreated | 2005-6-13 | lld:pubmed |
| pubmed-article:15845540 | pubmed:abstractText | Although hypoxia and transforming growth factor-beta (TGF-beta) inhibit differentiation of adipocytes from preadipocytes and bone marrow-derived cells in several species, the relationship between hypoxia and TGF-beta signaling in adipocytogenesis is unknown. In this study, we evaluated the mechanisms of inhibition of adipocyte differentiation by hypoxia and TGF-beta in human and murine marrow stromal cells (MSCs) and the role of TGF-beta/Smad signaling in the inhibition of adipocytogenesis by hypoxia. Both hypoxia-mimetic deferoxamine mesylate (DFO) and TGF-beta1 inhibited adipocyte differentiation (1.0% versus the control at 15 microm DFO and 1.4% versus the control at 1 ng/ml TGF-beta1) and adipocyte gene expression (peroxisome proliferator-activated receptor-gamma2 and lipoprotein lipase) in human MSCs after 21 days of treatment. Hypoxia (2% O(2)) and DFO (but not TGF-beta1) increased hypoxia-inducible factor-1alpha as shown by Western blotting. Macroarrays and Western and Northern blot analyses showed that hypoxia activated the TGF-beta/Smad signaling pathway and that both hypoxia and TGF-beta1 modulated adipocyte differentiation pathways such as the insulin-, peroxisome proliferator-activated receptor-gamma-, phosphatidylinositol 3-kinase-, and MAPK-associated signaling pathways. Studies with mouse marrow stromal cell lines derived from Smad3(+/+) or Smad3(-/-) mice revealed that the TGF-beta type I receptor (ALK-5) and its intracellular signaling molecule Smad3 were necessary for the inhibition of adipocyte differentiation by both TGF-beta and hypoxia-mimetic DFO. Thus, the TGF-beta/Smad signaling pathway is required for hypoxia-mediated inhibition of adipocyte differentiation in MSCs. | lld:pubmed |
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| pubmed-article:15845540 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15845540 | pubmed:citationSubset | IM | lld:pubmed |
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