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Sphingosine 1-Phosphate Receptor Blockade Affects Pro-Inflammatory Bone Marrow-Derived Macrophages and Relieves Mouse
Jingjing Yang1, Na Chang2, Le Yang3
1Department of Cell Biology, Municipal Laboratory for Liver Protection and Regulation of Regeneration, Capital Medical University, Beijing 100069, China. yangjingjing@zzu.edu.cn.
International Journal of Molecular Sciences
|September 25, 2019
Summary
Blocking sphingosine 1-phosphate receptors (S1PRs) reduces inflammation and liver injury in fatty liver disease. This targeted anti-inflammatory approach shows potential for treating fatty liver injury.
Area of Science:
- Hepatology
- Immunology
- Pharmacology
Background:
- Fatty liver injury, marked by fat accumulation, is a global health concern with limited effective treatments.
- Inflammation, involving macrophages, is a key pathological process in liver injury.
- Sphingosine 1-phosphate receptors (S1PRs) are implicated in inflammatory responses within the liver.
Purpose of the Study:
- To investigate the role of S1PRs in fatty liver injury.
- To determine if blocking S1PR subtypes 2 and 3 (S1PR2/3) can ameliorate fatty liver injury.
Main Methods:
- A methionine-choline-deficient and high-fat (MCDHF) diet induced fatty liver injury in mice.
- Macrophage populations were quantified using flow cytometry.
- Gene expression of inflammatory factors and S1PRs was analyzed via RT-qPCR and cytometric bead array.
Main Results:
- MCDHF diet elevated pro-inflammatory factors, S1P levels, and S1PR2/3 expression in the liver.
- Increased S1P and S1PR2/3 correlated positively with pro-inflammatory factor levels.
- S1PR2/3 blockade reduced pro-inflammatory macrophages (iMφ), inflammation, and liver injury/fibrosis, without altering fat accumulation.
Conclusions:
- The S1P/S1PR2/3 axis plays a significant role in mediating inflammation in fatty liver injury.
- Targeting S1PR2/3 with blockade offers a potential anti-inflammatory therapeutic strategy for fatty liver injury.
