| First Author | Lee HJ | Year | 2013 |
| Journal | Biochem Biophys Res Commun | Volume | 430 |
| Issue | 3 | Pages | 981-6 |
| PubMed ID | 23261458 | Mgi Jnum | J:193846 |
| Mgi Id | MGI:5469776 | Doi | 10.1016/j.bbrc.2012.11.127 |
| Citation | Lee HJ, et al. (2013) Angiopoietin-like protein 2, a chronic inflammatory mediator, is a new target induced by TGF-beta1 through a Smad3-dependent mechanism. Biochem Biophys Res Commun 430(3):981-6 |
| abstractText | Angiopoietin-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-beta1 has been reported to be augmented in obesity of rodents and humans, but inhibits adipocyte differentiation in vitro. Here we demonstrate that TGF-beta1 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-beta1 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-beta1-induced Angptl2 expression. These findings may provide insight into the molecular mechanisms of the increased expression of Angptl2 and TGF-beta1 in obesity. |
