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dc.contributor.authorLee, Hee Jae
dc.contributor.authorKim, Jun Hwan
dc.contributor.authorKim, Joon-Hyung
dc.contributor.authorMartinus, Ryan Dennis
dc.contributor.authorPark, Seok Hee
dc.coverage.spatialUnited Statesen_NZ
dc.date.accessioned2013-01-23T03:08:37Z
dc.date.available2013-01-23T03:08:37Z
dc.date.copyright2013-01
dc.date.issued2013
dc.identifier.citationLee, H. J., Kim, J. H., Kim, J.-H., Martinus, R. D., & Park, S. H. (2013). Angiopoietin-like protein 2, a chronic inflammatory mediator, is a new target induced by TGF-β1 through a Smad3-dependent mechanism. Biochemical and Biophysical Research Communications, 430(3), 981-986.en_NZ
dc.identifier.issn0006-291X
dc.identifier.urihttps://hdl.handle.net/10289/7097
dc.description.abstractAngiopoietin-like protein 2 (Angptl2) levels are increased by obesity and obesity-related pathological conditions, and it is considered to be an important adipocyte-derived inflammatory mediator. In contrast, the multifunctional cytokine TGF-β1 has been reported to be augmented in obesity of rodents and humans, but inhibits adipocyte differentiation in vitro. Here we demonstrate that TGF-β1 induces expression of the Angptl2 gene through a Smad3-dependent pathway in RAW264.7 macrophage cells, primary peritoneal macrophages, and differentiated 3T3-L1 adipocytes. Transcriptional induction of the Angptl2 gene by TGF-β1 was dependent on the Smad3 protein which binds to the Smad Binding Element (SBE) region located on the Angptl2 promoter. Macrophages with Smad3 knocked down by small interfering RNA showed reduction of TGF-β1-induced Angptl2 expression. These findings may provide insight into the molecular mechanisms of the increased expression of Angptl2 and TGF-β1 in obesity.en_NZ
dc.language.isoen
dc.publisherElsevieren_NZ
dc.relation.ispartofBiochemical and Biophysical Research Communications
dc.subjectAngptl2en_NZ
dc.subjectObesityen_NZ
dc.subjectSmad3en_NZ
dc.subjectTGF-β1en_NZ
dc.titleAngiopoietin-like protein 2, a chronic inflammatory mediator, is a new target induced by TGF-β1 through a Smad3-dependent mechanismen_NZ
dc.typeJournal Articleen_NZ
dc.identifier.doi10.1016/j.bbrc.2012.11.127en_NZ
dc.relation.isPartOfBiochemical and Biophysical Research Communicationsen_NZ
pubs.begin-page981en_NZ
pubs.elements-id38282
pubs.end-page986en_NZ
pubs.issue3en_NZ
pubs.volume430en_NZ


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