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Published on: December 26, 2016
Microglia-derived exosomes selective sorted by YB-1 alleviate nerve damage and cognitive outcome in Alzheimer's
Hong Wei1,2,3, Zhuzhi Zhu4, Yuhao Xu5
1Reproductive Center, The Fourth Affiliated Hospital of Jiangsu University, 20 Zhengdong Road, Zhenjiang, 212001, Jiangsu, P. R. China.
Background:
Neuroinflammation is a characteristic pathological change of Alzheimer's Diseases (AD). Microglia have been reported to participate in inflammatory responses within the central nervous system. However, the mechanism of microglia released exosome (EXO) contribute to communication within AD microenvironment remains obscure.
Methods:
The interaction between microglia and AD was investigated in vitro and in vivo. RNA-binding protein immunoprecipitation (RIP) was used to investigate the mechanisms of miR-223 and YB-1. The association between microglia derived exosomal YB-1/miR-223 axis and nerve cell damage were assessed using Western blot, immunofluorescence, RT-PCR, ELISA and wound healing assay.
Results:
Here, we reported AD model was responsible for the M1-like (pro-inflammatory) polarization of microglia which in turn induced nerve cell damage. While M2-like (anti-inflammatory) microglia could release miR-223-enriched EXO which reduced neuroinflammation and ameliorated nerve damage in AD model in vivo and in vitro. Moreover, YB-1 directly interacted with miR-223 both in cell and EXO, and participated in microglia exosomal miR-223 loading.
Conclusion:
These results indicate that anti-inflammatory microglia-mediated neuroprotection form inflammatory damage involves exporting miR-223 via EXO sorted by YB-1. Consequently, YB-1-mediated microglia exosomal sorting of miR-223 improved the nerve cell damage repair, representing a promising therapeutic target for AD.
Insights
Anti-inflammatory microglia release miR-223-enriched exosomes (EXO), mediated by YB-1, to reduce neuroinflammation and nerve damage in Alzheimer's Disease (AD). This YB-1/miR-223 axis offers a potential therapeutic target for AD.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Neuroinflammation is a key feature of Alzheimer's Disease (AD).
- Microglia play a role in central nervous system inflammatory responses.
- The precise role of microglia-derived exosomes (EXO) in AD intercellular communication is unclear.
Purpose of the Study:
- To investigate the interaction between microglia and AD.
- To elucidate the mechanism of microglia-derived exosomes in AD pathogenesis.
- To assess the therapeutic potential of the microglia-derived exosomal YB-1/miR-223 axis.
Main Methods:
- In vitro and in vivo AD models were utilized.
- RNA-binding protein immunoprecipitation (RIP) identified miR-223 and YB-1 interactions.
- Western blot, immunofluorescence, RT-PCR, ELISA, and wound healing assays assessed exosomal YB-1/miR-223 and nerve cell damage.
Main Results:
- AD models induced pro-inflammatory (M1-like) microglia polarization, causing nerve cell damage.
- Anti-inflammatory (M2-like) microglia released miR-223-enriched EXO, reducing neuroinflammation and nerve damage.
- YB-1 directly interacted with miR-223 and mediated its loading into microglia exosomes.
Conclusions:
- Anti-inflammatory microglia utilize YB-1 to export miR-223 via EXO, conferring neuroprotection.
- The YB-1-mediated exosomal sorting of miR-223 promotes nerve cell damage repair in AD.
- This pathway represents a promising therapeutic target for Alzheimer's Disease.
