Adipose tissue macrophages inhibit adipogenesis of mesenchymal precursor cells via wnt-5a in humans

In patients with obesity and type 2 diabetes, adipose tissue is infiltrated by macrophages known to alter adipogenesis of mesenchymal precursor cells via secretion of proinflammatory cytokines. Recently, it has been shown that under certain conditions, immune cells can also express wnt-5a, a factor...

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Published inInternational Journal of Obesity Vol. 35; no. 11; pp. 1450 - 1454
Main Authors Bilkovski, R, Schulte, D.M, Oberhauser, F, Mauer, J, Hampel, B, Gutschow, C, Krone, W, Laudes, M
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group 01.11.2011
Nature Publishing Group UK
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Summary:In patients with obesity and type 2 diabetes, adipose tissue is infiltrated by macrophages known to alter adipogenesis of mesenchymal precursor cells via secretion of proinflammatory cytokines. Recently, it has been shown that under certain conditions, immune cells can also express wnt-5a, a factor known to inhibit adipogenesis in humans. Therefore, in this study we aimed to investigate whether macrophages affect adipogenesis of mesenchymal precursor cells via wnt-5a. Wnt-5a was found to be expressed in adipose tissue macrophages in obese and type 2 diabetic human subjects in vivo by immunohistochemistry of adipose tissue biopsies. Furthermore, wnt-5a was detectable in circulating CD14+ blood monocytes of human subjects with obesity and type 2 diabetes on RNA level by real-time PCR. Besides expression analysis in vivo, we also performed functional studies to explore the role of wnt-5a in low-grade inflammation of adipose tissue. In a cell culture experiment, macrophage-conditioned differentiation medium inhibited adipogenesis of 3T3-L1 cells. This inhibitory effect was restored by adding neutralising anti-wnt-5a antibodies. In conclusion, our data indicate that macrophages alter adipogenesis of 3T3-L1 cells not only via classical proinflammatory cytokines, but also via wnt signalling molecules.
Bibliography:http://dx.doi.org/10.1038/ijo.2011.6
ObjectType-Article-1
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ISSN:0307-0565
1476-5497
DOI:10.1038/ijo.2011.6