Anti-inflammatory role of Gpnmb in adipose tissue of mice
Autor: | Nickl, Bernadette, Qadri, Fatimunnisa, Bader, Michael |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Inflammation
Liver Cirrhosis Mice Knockout Membrane Glycoproteins Macrophages Science Metabolic disorders Article Disease Models Animal Mice Adipose Tissue Gene Expression Regulation Cardiovascular and Metabolic Diseases Animals Medicine Obesity Disease Susceptibility Insulin Resistance Eye Proteins Biomarkers |
Zdroj: | Scientific Reports, Vol 11, Iss 1, Pp 1-10 (2021) Scientific Reports |
ISSN: | 2045-2322 |
Popis: | 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. |
Databáze: | OpenAIRE |
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