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Updated: Jul 13, 2025
Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
[Platelet-rich Plasma Induces M2 Macrophage Polarization via Regulating AMPK Singling Pathway]
Lin-Ying Shi1, Yan-Hui Li1, Jing-Jing Xu1
1Department of Blood Transfusion, General Hospital of Southern Theatre Command of PLA, Guangzhou 510010, Guangdong Province, China.
Objective:
To investigate the role of platelet-rich plasma (PRP) in inducing the M2 macrophage polarization via regulating AMPK singling pathway.
Methods:
The expressions of M1 marker CD11c and M2 marker CD206 in macrophages of blank control group, LPS group, LPS+PRP group, and LPS+PRP+Compound C group were detected by flow cytometry. Western blot was used to observe the effects of PRP on the expression of AMPK-mTOR signaling pathway-related proteins at different times (12 h, 18 h and 24 h) after LPS treatment. RNA interference technology was used to silence the expression of AMPK in macrophages, and the expression of TGF-β protein was subsequently examined by Western blot.
Results:
LPS significantly reduced the expression of CD206 and increased the expression of CD11c (P <0.05). After the addition of PRP, the expression of CD206 was significantly increased (P <0.05), while the expression of CD11c was significantly decreased (P <0.05). Compared with LPS group, PRP treatment significantly increased the expressions of p-AMPK and p-ULK1 proteins at 12 h, 18 h and 24 h, while significantly decreased the expression of p-mTOR protein (P <0.05). After the addition of AMPK inhibitor Compound C, the expression of CD206 was significantly reduced (P <0.05) and the expression of CD11c was significantly increased compared with LPS+PRP group (P <0.05). After silencing the expression of AMPK in macrophages, the promotion effect of PRP on TGF-β was significantly reduced (P <0.05).
Conclusion:
PRP can stimulate the transformation of macrophages to M2 type via AMPK signalling pathway.
Insights
Platelet-rich plasma (PRP) promotes M2 macrophage polarization by activating the AMPK signaling pathway. This study demonstrates PRP’s potential to modulate immune responses through macrophage differentiation.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Context:
- Macrophages play critical roles in immune responses, with M1 and M2 phenotypes exhibiting distinct functions.
- Lipopolysaccharide (LPS) is a potent inducer of M1 macrophage polarization.
- Platelet-rich plasma (PRP) is an autologous blood concentrate with therapeutic potential.
Purpose:
- To investigate the role of platelet-rich plasma (PRP) in inducing M2 macrophage polarization.
- To elucidate the involvement of the AMP-activated protein kinase (AMPK) signaling pathway in PRP-mediated macrophage polarization.
Summary:
- PRP treatment significantly increased M2 marker CD206 expression and decreased M1 marker CD11c expression in macrophages.
- PRP upregulated the phosphorylation of AMPK and ULK1 while downregulating mTOR phosphorylation, indicating activation of the AMPK pathway.
- Inhibition or silencing of AMPK abolished PRP's effect on M2 polarization and TGF-β expression.
Impact:
- PRP effectively promotes M2 macrophage polarization through the AMPK signaling pathway.
- This finding suggests a novel mechanism for PRP's immunomodulatory effects.
- PRP may serve as a therapeutic agent for conditions requiring M2 macrophage-driven resolution of inflammation.
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