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Published on: April 26, 2019
MicroRNA-26a-interleukin (IL)-6-IL-17 axis regulates the development of non-alcoholic fatty liver disease in a murine
1Department of Infectious Disease, and Laboratory of Liver Disease, Renmin Hospital, Hubei University of Medicine, China.
Abstract:
Non-alcoholic fatty liver disease (NAFLD) is a hepatic presentation of obesity and metabolic syndrome. MicroRNA 26a (Mir-26a) has been reported to play functions in cellular differentiation, cell growth, cell apoptosis and metastasis. A recent paper indicated that Mir-26a regulated insulin sensitivity and metabolism of glucose and lipids. However, the role of Mir-26a in NAFLD still needs to be investigated further. In our current study, vectors encoding pre-Mir-26a (LV-26a) and an empty lentiviral vector (LV-Con) delivered approximately 2 × 107 transforming units of recombinant lentivirus were injected into mice through the tail vein. LV-26a-infected mice were protected from glucose dysmetabolism and showed markedly decreased total liver weight, hepatic triglyceride deposition and serum alanine transaminase (ALT) concentration when compared with LV-Con-treated mice. LV-26a-treated mice also exhibited decreased infiltration of immune cells in the liver - something attributed to reduce infiltration of T cell receptor (TCR)-γδ+ , granulocyte-differentiation antigen-1 (Gr-1)+ cells and CD11b+ cells. Next, we found that Mir-26a inhibited the expression of interleukin (IL)-17 and IL-6 in vivo and in vitro. Furthermore, the decreased expression of IL-17 in the liver tissue induced by Mir-26a was abrogated completely by IL-6 overexpression. The decreased total liver weight, hepatic triglyceride deposition and serum ALT concentration induced by Mir-26a was also abrogated completely by IL-6 over-expression. In conclusion, the Mir-26a-IL-6-IL-17 axis regulates the development of NAFLD in a murine model.
Insights
MicroRNA 26a (Mir-26a) protects against non-alcoholic fatty liver disease (NAFLD) by reducing liver fat and inflammation. This study reveals Mir-26a regulates glucose and lipid metabolism via the IL-6 and IL-17 pathway.
Area of Science:
- Hepatology
- Molecular Biology
- Metabolic Syndrome
Background:
- Non-alcoholic fatty liver disease (NAFLD) is linked to obesity and metabolic syndrome.
- MicroRNA 26a (Mir-26a) influences cell processes and metabolism, but its role in NAFLD is unclear.
- Investigating Mir-26a's function in NAFLD is crucial for understanding disease mechanisms.
Purpose of the Study:
- To investigate the role of MicroRNA 26a (Mir-26a) in the development of non-alcoholic fatty liver disease (NAFLD).
- To elucidate the molecular mechanisms by which Mir-26a affects liver metabolism and inflammation in a murine model.
Main Methods:
- Lentiviral vectors encoding pre-Mir-26a (LV-26a) or control (LV-Con) were administered to mice.
- Mice were assessed for metabolic parameters, liver pathology, and immune cell infiltration.
- Gene and protein expression levels of cytokines, including IL-6 and IL-17, were analyzed in vivo and in vitro.
Main Results:
- LV-26a treatment reduced liver weight, hepatic triglyceride deposition, and serum ALT levels in mice.
- Mir-26a inhibited the infiltration of immune cells, specifically TCR-γδ+, Gr-1+, and CD11b+ cells.
- Mir-26a suppressed IL-6 and IL-17 expression; IL-6 overexpression abrogated Mir-26a's protective effects.
Conclusions:
- The Mir-26a-IL-6-IL-17 axis plays a significant role in regulating NAFLD development.
- Mir-26a demonstrates therapeutic potential for NAFLD by modulating metabolic and inflammatory pathways.
