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Mesenchymal stem cell-derived exosome miR-542-3p suppresses inflammation and prevents cerebral infarction
Guofeng Cai1, Guoliang Cai2,3, Haichun Zhou4
1Hanan Branch of Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, 150001, China. cangjiong1973@163.com.
Background:
Cerebral infarction ranks as the second leading cause of disability and death globally, and inflammatory response of glial cells is the main cause of brain damage during cerebral infarction.
Methods:
Studies have shown that mesenchymal stem cells (MSCs) can secrete exosomes and contribute to cerebral disease. Here, we would explore the function of MSC-derived exosome in cerebral infarction.
Results:
Microarray indicated a decrease of miR-542-3p and an increase of Toll-Like Receptor 4 (TLR4) in middle cerebral artery occlusion (MCAO) mice comparing with sham mice. And luciferase and RIP analysis indicated a binding of miR-542-3p and TLR4. Then, we injected AAV9-miR-542-3p into paracele of sham or MCAO mice. Functional analysis showed that AAV9-miR-542-3p inhibited infarction area and the number of degenerating neurons and suppressed inflammatory factors' expression and inflammatory cell infiltration. As well, transfection of miR-542-3p mimics into HA1800 cells underwent oxygen and glucose deprivation (OGD). Similarly, overexpression of miR-542-3p alleviated OGD induced cell apoptosis, ROS, and activation of inflammation response. Moreover, miR-542-3p could be packaged into MSCs and secreted into HA1800 cells. The extractive exosome-miR-21-3p treatment relieved MCAO- or OGD-induced cerebral injury and inflammation through targeting TLR4.
Conclusion:
These results confirmed that MSC-derived exosome miR-542-3p prevented ischemia-induced glial cell inflammatory response via inhibiting TLR4. These results suggest possible therapeutic strategies for using exosome delivery of miR-542-3p to cure cerebral ischemic injury.
Insights
Mesenchymal stem cell-derived exosomes carrying miR-542-3p protect against cerebral infarction by inhibiting Toll-Like Receptor 4 (TLR4) and reducing inflammation. This offers a potential therapy for ischemic brain injury.
Area of Science:
- Neuroscience
- Cell Biology
- Regenerative Medicine
Background:
- Cerebral infarction is a leading global cause of death and disability.
- Glial cell inflammatory response significantly contributes to brain damage in cerebral infarction.
Purpose of the Study:
- To investigate the therapeutic function of mesenchymal stem cell (MSC)-derived exosomes in cerebral infarction.
- To explore the role of microRNA-542-3p (miR-542-3p) and Toll-Like Receptor 4 (TLR4) in MSC-mediated neuroprotection.
Main Methods:
- Microarray analysis identified altered miR-542-3p and TLR4 levels in a mouse model of cerebral infarction (MCAO).
- Luciferase and RIP assays confirmed the binding interaction between miR-542-3p and TLR4.
- Adeno-associated virus (AAV9) carrying miR-542-3p was administered to MCAO mice; miR-542-3p mimics were used in oxygen-glucose deprivation (OGD) cell models.
- Exosomes derived from MSCs engineered to carry miR-542-3p were tested for therapeutic effects.
Main Results:
- Overexpression of miR-542-3p via AAV9 injection reduced infarct volume, neuronal degeneration, and neuroinflammation in MCAO mice.
- miR-542-3p mimics alleviated OGD-induced apoptosis, reactive oxygen species (ROS), and inflammation in neuronal cells.
- MSC-derived exosomes containing miR-542-3p effectively mitigated MCAO- and OGD-induced cerebral injury and inflammation by targeting TLR4.
Conclusions:
- MSC-derived exosome miR-542-3p exerts a protective effect against ischemia-induced brain injury by suppressing glial cell inflammatory responses through TLR4 inhibition.
- Exosome-mediated delivery of miR-542-3p represents a promising therapeutic strategy for treating cerebral ischemic injury.
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