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Ring finger protein 10 is atherosclerosis protective and modulates macrophage polarization
Ke-Xin Zhao1, Shu-Xu Jin2, Ming-Hao Li1
1Cardiology I, Beidahuang Group General Hospital, No. 235, Hashuang Road, Nangang District, Harbin 150006, Heilongjiang, P.R. China.
Experimental Animals
|December 3, 2025
Summary
Ring finger protein 10 (RNF10) plays an anti-atherosclerotic role by suppressing pro-inflammatory M1 macrophages and promoting anti-inflammatory M2 macrophages. This suggests RNF10 is a potential therapeutic target for atherosclerosis.
Area of Science:
- Immunology
- Cardiovascular Biology
- Molecular Biology
Background:
- Macrophages exhibit plasticity, differentiating into pro-inflammatory M1 or anti-inflammatory M2 phenotypes.
- Macrophage polarization dynamics are crucial in the progression of atherosclerosis.
- The specific role of Ring finger protein 10 (RNF10) in macrophage polarization during atherosclerosis requires elucidation.
Purpose of the Study:
- To investigate the function of RNF10 in regulating macrophage polarization in the context of atherosclerosis.
- To determine the impact of RNF10 on M1 and M2 macrophage markers and foam cell formation.
Main Methods:
- Generated macrophage-specific RNF10-deficient ApoE-/- mice (RNF10Mac-KO/ApoE-/-) and control littermates (RNF10fl/fl/ApoE-/-) fed a high-fat diet.
- Isolated peritoneal macrophages and utilized RAW264.7 murine macrophages for in vitro studies.
- Manipulated RNF10 expression via overexpression vectors and small interfering RNA (siRNA) in macrophages.
- Stimulated macrophages with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation and assessed M1/M2 marker expression.
Main Results:
- RNF10Mac-KO/ApoE-/- mice exhibited exacerbated atherosclerotic lesions, increased resident macrophages, elevated M1 marker (iNOS) expression, and reduced M2 marker (Arginase-1) expression compared to controls.
- RNF10 overexpression in macrophages suppressed M1 markers (IL-1β, IL-6, iNOS) and enhanced M2 markers (IL-10, Arg-1).
- RNF10 overexpression attenuated lipid accumulation in ox-LDL-induced foam cells, while RNF10 silencing promoted it.
Conclusions:
- RNF10 deficiency in macrophages exacerbates atherosclerosis, characterized by a shift towards a pro-inflammatory M1 phenotype.
- RNF10 promotes an anti-inflammatory M2 macrophage phenotype and reduces foam cell formation.
- RNF10 in macrophages possesses a protective, anti-atherosclerotic role, suggesting its therapeutic potential.
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