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Ablation of myeloid discoidin domain receptor 2 exacerbates arthritis and high fat diet induced inflammation
Qingyun Liu1, Xiaolong Wang2, Yazhuo Chen1
1Center for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.
Abstract:
Chronic systemic inflammation leads to sever disorders and diseases. It is of great importance to explore novel target for effective treatment. Discoidin domain receptor 2 (Ddr2) is a member of receptor tyrosine kinase (RTK) family and is implicated in skeletal and fat hemostasis. However, the role of Ddr2 in myeloid cells remains obscure. In this study, we conditionally deleted Ddr2 in myeloid lineage cells to generate cKO mice to investigate the role of Ddr2 in myeloid lineage cells. We found that cKO mice exhibited more severe inflammation both in collagen antibody-induced arthritis (CAIA) and high-fat diet (HFD)-induced obesity, indicating the protective role of Ddr2 against inflammation. Mechanistically, Ddr2 promotes macrophage repolarization from the M1 to M2 phenotype, and protect against systemic inflammation. Our study reveals for the first time that Ddr2 modulates macrophage repolarization and plays critical roles in macrophage-mediated inflammation, providing potential target for the intervention of inflammation and related diseases.
Insights
Discoidin domain receptor 2 (Ddr2) protects against inflammation by promoting macrophage repolarization. Deleting Ddr2 in myeloid cells worsened inflammatory diseases, highlighting Ddr2 as a therapeutic target.
Area of Science:
- Immunology
- Cell Biology
- Molecular Medicine
Background:
- Chronic systemic inflammation underlies numerous severe disorders.
- Identifying novel therapeutic targets for inflammation is crucial.
- The function of Discoidin domain receptor 2 (Ddr2) in myeloid cells is largely unknown.
Purpose of the Study:
- To investigate the role of Ddr2 in myeloid lineage cells.
- To determine the impact of Ddr2 deficiency on inflammatory conditions.
Main Methods:
- Conditional knockout (cKO) mice lacking Ddr2 in myeloid cells were generated.
- Inflammatory responses were assessed in collagen antibody-induced arthritis (CAIA) and high-fat diet (HFD)-induced obesity models.
Main Results:
- Ddr2-deficient mice showed exacerbated inflammation in both CAIA and HFD models.
- Ddr2 was found to promote macrophage repolarization from the M1 to M2 phenotype.
- This repolarization conferred protection against systemic inflammation.
Conclusions:
- Ddr2 plays a critical protective role against systemic inflammation.
- Ddr2 modulates macrophage repolarization, impacting inflammation.
- Ddr2 represents a potential therapeutic target for inflammatory diseases.
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