Hematopoietic cyclooxygenase-2 deficiency increases adipose tissue inflammation and adiposity in obesity

Obesity
Nikhil AdiViswanathan Saraswathi

Abstract

Adipose tissue (AT) macrophages mediate AT inflammation in obesity, and cyclooxygenase-2 (COX-2) is a major inflammatory gene. It was hypothesized that deletion of hematopoietic COX-2 will inhibit AT inflammation in obesity. Lethally irradiated wild-type (WT) mice were injected with bone marrow (BM) cells collected from WT or COX-2 knock-out (COX-2-/-) donor mice and fed a high-fat diet for 16 weeks. The mice that received BM cells from COX-2-/- mice (BM-COX-2-/-) gained increased body weight, fat mass, and visceral AT (VAT) mass. These mice exhibited reduced inflammatory markers in the VAT stromal vascular cells (SVC). However, the inflammatory markers were increased in adipocyte fraction and/or whole VAT. The activation of ERK1/2 MAPK, a pro-inflammatory signaling pathway, was increased in BM-COX-2-/- mice. The molecular markers of adipogenesis were increased in the VAT or adipocyte fraction. Wnt signaling markers which inhibit adipogenesis, including Wnt3A and DVL3, were reduced, and Wnt5a/b which promotes inflammation was increased in the VAT and/or adipocytes. Finally, an increase in hepatic triglyceride levels in BM-COX-2-/- mice was noted. The data suggest that COX-2 deletion in hematopoietic cells reduces SVC inflammati...Continue Reading

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Citations

Dec 23, 2015·Biochemical and Biophysical Research Communications·Viswanathan SaraswathiAlexander V Kabanov
May 28, 2021·Journal of Cellular and Molecular Medicine·Xiaobo NieWei-Dong Chen

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