Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice
Single-nucleotide polymorphisms within major histocompatibility class II (MHC II) genes have been associated with an increased risk of drug-induced liver injury. However, it has never been addressed whether the MHC II pathway plays an important role in the development of nonalcoholic fatty liver dis...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | International Journal of Endocrinology |
| Online Access: | http://dx.doi.org/10.1155/2013/972962 |
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| author | Gilles Willemin Catherine Roger Armelle Bauduret Kaori Minehira |
| author_facet | Gilles Willemin Catherine Roger Armelle Bauduret Kaori Minehira |
| author_sort | Gilles Willemin |
| collection | DOAJ |
| description | Single-nucleotide polymorphisms within major histocompatibility class II (MHC II) genes have been associated with an increased risk of drug-induced liver injury. However, it has never been addressed whether the MHC II pathway plays an important role in the development of nonalcoholic fatty liver disease, the most common form of liver disease.
We used a mouse model that has a complete knockdown of genes in the MHC II pathway (MHCIIΔ/Δ). Firstly we studied the effect of high-fat diet-induced hepatic inflammation in these mice. Secondly we studied the development of carbon-tetra-chloride- (CCl4-) induced hepatic cirrhosis. After the high-fat diet, both groups developed obesity and hepatic steatosis with a similar degree of hepatic inflammation, suggesting no impact of the knockdown of MHC II on high-fat diet-induced inflammation in mice. In the second study, we confirmed that the CCl4 injection significantly upregulated the MHC II genes in wild-type mice. The CCl4 treatment significantly induced genes related to the fibrosis formation in wild-type mice, whereas this was lower in MHCIIΔ/Δ mice. The liver histology, however, showed no detectable difference between groups, suggesting that the MHC II pathway is not required for the development of hepatic fibrosis induced by CCl4. |
| format | Article |
| id | doaj-art-6c2dd5b77db541dc9cee9a272a804476 |
| institution | Kabale University |
| issn | 1687-8337 1687-8345 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Endocrinology |
| spelling | doaj-art-6c2dd5b77db541dc9cee9a272a8044762025-02-03T06:00:11ZengWileyInternational Journal of Endocrinology1687-83371687-83452013-01-01201310.1155/2013/972962972962Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in MiceGilles Willemin0Catherine Roger1Armelle Bauduret2Kaori Minehira3Department of Physiology, University of Lausanne, Rue du Bugnon 7, 1005 Lausanne, SwitzerlandCenter for Integrative Genomics, University of Lausanne, 1010 Lausanne, SwitzerlandCenter for Integrative Genomics, University of Lausanne, 1010 Lausanne, SwitzerlandDepartment of Physiology, University of Lausanne, Rue du Bugnon 7, 1005 Lausanne, SwitzerlandSingle-nucleotide polymorphisms within major histocompatibility class II (MHC II) genes have been associated with an increased risk of drug-induced liver injury. However, it has never been addressed whether the MHC II pathway plays an important role in the development of nonalcoholic fatty liver disease, the most common form of liver disease. We used a mouse model that has a complete knockdown of genes in the MHC II pathway (MHCIIΔ/Δ). Firstly we studied the effect of high-fat diet-induced hepatic inflammation in these mice. Secondly we studied the development of carbon-tetra-chloride- (CCl4-) induced hepatic cirrhosis. After the high-fat diet, both groups developed obesity and hepatic steatosis with a similar degree of hepatic inflammation, suggesting no impact of the knockdown of MHC II on high-fat diet-induced inflammation in mice. In the second study, we confirmed that the CCl4 injection significantly upregulated the MHC II genes in wild-type mice. The CCl4 treatment significantly induced genes related to the fibrosis formation in wild-type mice, whereas this was lower in MHCIIΔ/Δ mice. The liver histology, however, showed no detectable difference between groups, suggesting that the MHC II pathway is not required for the development of hepatic fibrosis induced by CCl4.http://dx.doi.org/10.1155/2013/972962 |
| spellingShingle | Gilles Willemin Catherine Roger Armelle Bauduret Kaori Minehira Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice International Journal of Endocrinology |
| title | Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice |
| title_full | Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice |
| title_fullStr | Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice |
| title_full_unstemmed | Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice |
| title_short | Major Histocompatibility Class II Pathway Is Not Required for the Development of Nonalcoholic Fatty Liver Disease in Mice |
| title_sort | major histocompatibility class ii pathway is not required for the development of nonalcoholic fatty liver disease in mice |
| url | http://dx.doi.org/10.1155/2013/972962 |
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