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Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
MRP8/14 mediates macrophage efferocytosis through RAGE and Gas6/MFG-E8, and induces polarization via TLR4-dependent
Kangxin Li1, Guiming Chen1, Haihua Luo1
1Guangdong Provincial Key Laboratory of Proteomics, State Key Laboratory of Organ Failure Research, Department of Pathophysiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Abstract:
Myeloid-related protein 8/14 (MRP8/14) participates in various inflammatory responses, however, its effect on macrophage efferocytosis remains unclear. Here, we demonstrate that MRP8/14 significantly inhibits the efferocytosis of apoptotic thymocytes by mouse bone marrow-derived macrophages (BMDMs), which later proves to be associated with the receptor for advanced glycation end products (RAGE) or for reducing the expression of growth arrest-specific protein 6 and milk fat globule epidermal growth factor 8, independent of RAGE. Furthermore, MRP8/14 promotes polarization of BMDMs from the M2 - to M1 -like phenotype by upregulating expression of M1 -related surface receptor proteins and signature M1 -marker genes and by downregulating signature M2 -marker gene expression, which depends on Toll-like receptor 4 and p38 mitogen-activated protein kinase/nuclear factor κB pathways. Thus, we report a significant inhibitory effect of MRP8/14 on macrophage efferocytosis and MRP8/14-mediated phenotypic polarization, which may be helpful in developing novel therapeutic strategies leading to inflammation resolution.
Insights
Myeloid-related protein 8/14 (MRP8/14) inhibits macrophage efferocytosis and promotes M1 polarization, impacting inflammation resolution. This study clarifies MRP8/14
Area of Science:
- Immunology
- Cell Biology
Background:
- Myeloid-related protein 8/14 (MRP8/14) is involved in inflammatory processes.
- The precise role of MRP8/14 in macrophage efferocytosis is not well understood.
Purpose of the Study:
- To investigate the effect of MRP8/14 on macrophage efferocytosis.
- To explore the impact of MRP8/14 on macrophage polarization.
- To elucidate the molecular mechanisms underlying MRP8/14's actions.
Main Methods:
- Utilized mouse bone marrow-derived macrophages (BMDMs) to assess efferocytosis.
- Investigated the expression of key surface receptors and marker genes.
- Analyzed the involvement of Toll-like receptor 4 (TLR4) and p38 MAPK/NF-κB pathways.
Main Results:
- MRP8/14 significantly inhibited the efferocytosis of apoptotic thymocytes by BMDMs.
- MRP8/14 promoted M2 to M1-like macrophage polarization.
- Inhibition of efferocytosis was linked to reduced expression of GAS6 and MFG-E8, independent of RAGE.
- Macrophage polarization was dependent on TLR4 and p38 MAPK/NF-κB signaling.
Conclusions:
- MRP8/14 plays a crucial role in suppressing macrophage efferocytosis.
- MRP8/14 drives M1-like polarization of macrophages.
- Findings suggest MRP8/14 as a potential therapeutic target for modulating inflammation.
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