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| Item Type: | Article |
|---|---|
| Title: | Anti-inflammatory role of Gpnmb in adipose tissue of mice |
| Creators Name: | Nickl, B. and Qadri, F. and Bader, M. |
| Abstract: | Obesity can cause a chronic, low-grade inflammation, which is a critical step in the development of type II diabetes and cardiovascular diseases. Inflammation is associated with the expression of glycoprotein nonmetastatic melanoma protein b (Gpnmb), which is mainly expressed by macrophages and dendritic cells. We generated a Gpnmb-knockout mouse line using Crispr-Cas9 to assess the role of Gpnmb in a diet-induced obesity. The absence of Gpnmb did not affect body weight gain and blood lipid parameters. While wildtype animals became obese but remained otherwise metabolically healthy, Gpnmb-knockout animals developed, in addition to obesity, symptoms of metabolic syndrome such as adipose tissue inflammation, insulin resistance and liver fibrosis. We observed a strong Gpnmb expression in adipose tissue macrophages in wildtype animals and a decreased expression of most macrophage-related genes independent of their inflammatory function. This was corroborated by in vitro data showing that Gpnmb was mostly expressed by reparative macrophages while only pro-inflammatory stimuli induced shedding of Gpnmb. The data suggest that Gpnmb is ameliorating adipose tissue inflammation independent of the polarization of macrophages. Taken together, the data suggest an immune-balancing function of Gpnmb that could delay the metabolic damage caused by the induction of obesity. |
| Keywords: | Adipose Tissue, Biomarkers, Animal Disease Models, Disease Susceptibility, Eye Proteins, Gene Expression Regulation, Inflammation, Insulin Resistance, Liver Cirrhosis, Macrophages, Membrane Glycoproteins, Knockout Mice, Animals, Mice |
| Source: | Scientific Reports |
| ISSN: | 2045-2322 |
| Publisher: | Nature Publishing Group |
| Volume: | 11 |
| Number: | 1 |
| Page Range: | 19614 |
| Date: | 4 October 2021 |
| Official Publication: | https://doi.org/10.1038/s41598-021-99090-6 |
| PubMed: | View item in PubMed |
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