| First Author | Roth Flach RJ | Year | 2013 |
| Journal | J Biol Chem | Volume | 288 |
| Issue | 4 | Pages | 2882-92 |
| PubMed ID | 23235150 | Mgi Jnum | J:315500 |
| Mgi Id | MGI:6829090 | Doi | 10.1074/jbc.M112.412346 |
| Citation | Roth Flach RJ, et al. (2013) beta3-Adrenergic receptor stimulation induces E-selectin-mediated adipose tissue inflammation. J Biol Chem 288(4):2882-92 |
| abstractText | Inflammation induced by wound healing or infection activates local vascular endothelial cells to mediate leukocyte rolling, adhesion, and extravasation by up-regulation of leukocyte adhesion molecules such as E-selectin and P-selectin. Obesity-associated adipose tissue inflammation has been suggested to cause insulin resistance, but weight loss and lipolysis also promote adipose tissue immune responses. While leukocyte-endothelial interactions are required for obesity-induced inflammation of adipose tissue, it is not known whether lipolysis-induced inflammation requires activation of endothelial cells. Here, we show that beta(3)-adrenergic receptor stimulation by CL 316,243 promotes adipose tissue neutrophil infiltration in wild type and P-selectin-null mice but not in E-selectin-null mice. Increased expression of adipose tissue cytokines IL-1beta, CCL2, and TNF-alpha in response to CL 316,243 administration is also dependent upon E-selectin but not P-selectin. In contrast, fasting increases adipose-resident macrophages but not neutrophils, and does not activate adipose-resident endothelium. Thus, two models of lipolysis-induced inflammation induce distinct immune cell populations within adipose tissue and exhibit distinct dependences on endothelial activation. Importantly, our results indicate that beta(3)-adrenergic stimulation acts through up-regulation of E-selectin in adipose tissue endothelial cells to induce neutrophil infiltration. |
