Journal
CELL REPORTS
Volume 31, Issue 13, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2020.107818
Keywords
-
Categories
Funding
- National Institutes of Health, United States [HL092969, AI125378, AI130280, DK122662]
- University of Washington Nutrition Obesity Research Center [DK035816]
- University of Washington [HL092969]
- University of Washington School of Pharmacy Mass Spectrometry Center
Ask authors/readers for more resources
Obesity is characterized by adipose tissue inflammation. Because proteoglycans regulate inflammation, here we investigate their role in adipose tissue inflammation in obesity. We find that adipose tissue versican and biglycan increase in obesity. Versican is produced mainly by adipocytes and biglycan by adipose tissue macrophages. Both proteoglycans are also present in adipose tissue from obese human subjects undergoing gastric bypass surgery. Deletion of adipocyte-specific versican or macrophage-specific biglycan in mice reduces macrophage accumulation and chemokine and cytokine expression, although only adipocyte-specific versican deletion leads to sustained improvement in glucose tolerance. Macrophage-derived biglycan activates inflammatory genes in adipocytes. Versican expression increases in cultured adipocytes exposed to excess glucose, and adipocyte-conditioned medium stimulates inflammation in resident peritoneal macrophages, in part because of a versican breakdown product, versikine. These findings provide insights into the role of adipocyte- and macrophage-derived proteoglycans in adipose tissue inflammation in obesity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available