The Role of STING in Liver Injury Is Both Stimulus- and Time-Dependent
STING, <i>Tmem173</i>, is involved in liver injury caused by both infectious and sterile inflammatory models. Its role in toxic liver injury and non-alcoholic fatty liver disease (NAFLD), however, is less clear. While a few groups have investigated its role in NAFLD pathogenesis, results...
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MDPI AG
2022-09-01
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Online Access: | https://www.mdpi.com/2072-6643/14/19/4029 |
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author | Kevin Siao Dounia Le Guillou Jacquelyn J. Maher Caroline C. Duwaerts |
author_facet | Kevin Siao Dounia Le Guillou Jacquelyn J. Maher Caroline C. Duwaerts |
author_sort | Kevin Siao |
collection | DOAJ |
description | STING, <i>Tmem173</i>, is involved in liver injury caused by both infectious and sterile inflammatory models. Its role in toxic liver injury and non-alcoholic fatty liver disease (NAFLD), however, is less clear. While a few groups have investigated its role in NAFLD pathogenesis, results have been conflicting. The objective of this study was to clarify the exact role of STING in toxic liver injury and NAFLD models. Goldenticket mice (<i>Tmem173<sup>gt</sup></i>), which lack STING protein, were subjected to either a toxic liver injury with tunicamycin (TM) or one of two dietary models of non-alcoholic fatty liver disease: high fructose feeding or Fructose-Palmitate-Cholesterol (FPC) feeding. Three days after TM injection, <i>Tmem173<sup>gt</sup></i> mice demonstrated less liver injury (average ALT of 54 ± 5 IU/L) than control mice (average ALT 108 ± 24 IU/L). In contrast, no significant differences in liver injury were seen between WT and <i>Tmem173<sup>gt</sup></i> mice fed either high fructose or FPC. <i>Tmem173<sup>gt</sup></i> mice only distinguished themselves from WT mice in their increased insulin resistance. In conclusion, while STING appears to play a role in toxic liver injury mediated by TM, it plays little to no role in two dietary models of NAFLD. The exact role of STING appears to be stimulus-dependent. |
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issn | 2072-6643 |
language | English |
last_indexed | 2024-03-09T21:20:23Z |
publishDate | 2022-09-01 |
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series | Nutrients |
spelling | doaj.art-ff478c1b319f4986a799cc6b5553f6552023-11-23T21:24:21ZengMDPI AGNutrients2072-66432022-09-011419402910.3390/nu14194029The Role of STING in Liver Injury Is Both Stimulus- and Time-DependentKevin Siao0Dounia Le Guillou1Jacquelyn J. Maher2Caroline C. Duwaerts3Department of Medicine, University of California, San Francisco, CA 94143, USADepartment of Medicine, University of California, San Francisco, CA 94143, USADepartment of Medicine, University of California, San Francisco, CA 94143, USADepartment of Medicine, University of California, San Francisco, CA 94143, USASTING, <i>Tmem173</i>, is involved in liver injury caused by both infectious and sterile inflammatory models. Its role in toxic liver injury and non-alcoholic fatty liver disease (NAFLD), however, is less clear. While a few groups have investigated its role in NAFLD pathogenesis, results have been conflicting. The objective of this study was to clarify the exact role of STING in toxic liver injury and NAFLD models. Goldenticket mice (<i>Tmem173<sup>gt</sup></i>), which lack STING protein, were subjected to either a toxic liver injury with tunicamycin (TM) or one of two dietary models of non-alcoholic fatty liver disease: high fructose feeding or Fructose-Palmitate-Cholesterol (FPC) feeding. Three days after TM injection, <i>Tmem173<sup>gt</sup></i> mice demonstrated less liver injury (average ALT of 54 ± 5 IU/L) than control mice (average ALT 108 ± 24 IU/L). In contrast, no significant differences in liver injury were seen between WT and <i>Tmem173<sup>gt</sup></i> mice fed either high fructose or FPC. <i>Tmem173<sup>gt</sup></i> mice only distinguished themselves from WT mice in their increased insulin resistance. In conclusion, while STING appears to play a role in toxic liver injury mediated by TM, it plays little to no role in two dietary models of NAFLD. The exact role of STING appears to be stimulus-dependent.https://www.mdpi.com/2072-6643/14/19/4029NASHSTINGFPC dietinsulin resistancetoxic liver injury |
spellingShingle | Kevin Siao Dounia Le Guillou Jacquelyn J. Maher Caroline C. Duwaerts The Role of STING in Liver Injury Is Both Stimulus- and Time-Dependent Nutrients NASH STING FPC diet insulin resistance toxic liver injury |
title | The Role of STING in Liver Injury Is Both Stimulus- and Time-Dependent |
title_full | The Role of STING in Liver Injury Is Both Stimulus- and Time-Dependent |
title_fullStr | The Role of STING in Liver Injury Is Both Stimulus- and Time-Dependent |
title_full_unstemmed | The Role of STING in Liver Injury Is Both Stimulus- and Time-Dependent |
title_short | The Role of STING in Liver Injury Is Both Stimulus- and Time-Dependent |
title_sort | role of sting in liver injury is both stimulus and time dependent |
topic | NASH STING FPC diet insulin resistance toxic liver injury |
url | https://www.mdpi.com/2072-6643/14/19/4029 |
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