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Title: | RAGE deficiency does not affect non-alcoholic steatohepatitis and atherosclerosis in Western type diet-fed Ldlr(-/-) mice | Authors: | Bijnen, Mitchell Beelen, Nicky WETZELS, Suzan van De Gaar, Jose Vroomen, Maria Wijnands, Erwin Scheijen, Jean L. van de Waarenburg, Marjo P. H. Gijbels, Marion J. Cleutjens, Jack P. Biessen, Erik A. L. Stehouwer, Coen D. A. Schalkwijk, Casper G. WOUTERS, Kristiaan |
Issue Date: | 2018 | Publisher: | NATURE PUBLISHING GROUP | Source: | SCIENTIFIC REPORTS, 8 (Art N° 15256) | Abstract: | Non-alcoholic fatty liver disease is a spectrum of liver diseases ranging from steatosis only to non-alcoholic steatohepatitis (NASH). The latter is characterized by hepatic inflammation, which increases the risk of cardiovascular disease. It is poorly understood which factors contribute to the onset of hepatic inflammation characterizing the progression from steatosis to NASH. Previously, we demonstrated increased advanced glycation endproducts (AGEs) in the livers of NASH patients. We hypothesise that AGEs play a key role in NASH development by activating their proinflammatory receptor, RAGE. RAGE-deficient mice and wildtype littermates, both on Ldlr(-/-) background, were fed a Western type diet (WTD) for 3 or 12 weeks. Flow cytometry, histology, gene expression and AGE measurements were performed to evaluate the effects of RAGE deficiency. RAGE-deficient mice displayed reduced weight gain and visceral fat expansion compared to control mice. No difference in adipose tissue inflammation was observed between groups. RAGE deficiency did not affect WTD-induced monocytosis, circulating lipids or hepatic steatosis. WTD-induced hepatic neutrophil and macrophage accumulation and atherosclerotic plaque development was comparable between control and RAGE-deficient mice. No difference in AGE levels was observed. RAGE does not seem to play a major role in the development of NASH or atherosclerosis in a hyperlipidemic mouse model. | Notes: | [Bijnen, Mitchell; Beelen, Nicky; Wetzels, Suzan; van De Gaar, Jose; Vroomen, Maria; Scheijen, Jean L.; van de Waarenburg, Marjo P. H.; Stehouwer, Coen D. A.; Schalkwijk, Casper G.; Wouters, Kristiaan] MUMC, Dept Internal Med, Maastricht, Netherlands. [Bijnen, Mitchell; Beelen, Nicky; Wetzels, Suzan; van De Gaar, Jose; Vroomen, Maria; Wijnands, Erwin; Scheijen, Jean L.; van de Waarenburg, Marjo P. H.; Gijbels, Marion J.; Cleutjens, Jack P.; Biessen, Erik A. L.; Stehouwer, Coen D. A.; Schalkwijk, Casper G.; Wouters, Kristiaan] MUMC, CARIM, Maastricht, Netherlands. [Wetzels, Suzan] Hasselt Univ, Biomed Res Inst, Dept Immunol & Biochem, Hasselt, Belgium. [Wijnands, Erwin; Gijbels, Marion J.; Cleutjens, Jack P.; Biessen, Erik A. L.] MUMC, Dept Pathol, Maastricht, Netherlands. [Gijbels, Marion J.] MUMC, Dept Mol Genet, Maastricht, Netherlands. [Gijbels, Marion J.] AMC, Dept Med Biochem, Expt Vasc Biol, Amsterdam, Netherlands. | Document URI: | http://hdl.handle.net/1942/28845 | ISSN: | 2045-2322 | e-ISSN: | 2045-2322 | DOI: | 10.1038/s41598-018-33661-y | ISI #: | 000447318500011 | Rights: | Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Te images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ | Category: | A1 | Type: | Journal Contribution | Validations: | ecoom 2019 |
Appears in Collections: | Research publications |
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