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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Astrocyte-derived exosomes enriched with miR-873a-5p inhibit neuroinflammation via microglia phenotype modulation
Xiaobing Long1, Xiaolong Yao1, Qian Jiang1
1Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Background:
The interaction between astrocytes and microglia plays a vital role in the damage and repair of brain lesions due to traumatic brain injury (TBI). Recent studies have shown that exosomes act as potent mediators involved in intercellular communication.
Methods:
In the current study, the expression of inflammatory factors and miR-873a-5p in the lesion area and oedema area was evaluated in 15 patients with traumatic brain injury. Exosomes secreted by astrocytes were detected by immunofluorescence, Western blot and electron microscopy. A mouse model of TBI and an in vitro model of LPS-induced primary microglia were established to study the protective mechanism of exosomes from miR-873a-5p overexpressing in TBI-induced nerve injury.
Results:
We discovered that exosomes derived from activated astrocytes promote microglial M2 phenotype transformation following TBI. More than 100 miRNAs were detected in these astrocyte-derived exosomes. miR-873a-5p is a major component that was highly expressed in human traumatic brain tissue. Moreover, miR-873a-5p significantly inhibited LPS-induced microglial M1 phenotype transformation and the subsequent inflammation through decreased phosphorylation of ERK and NF-κB p65. This effect also greatly improved the modified neurological severity score (mNSS) and attenuated brain injury in a strictly controlled cortical impact mouse model.
Conclusions:
Taken together, our research indicates that miRNAs in the exosomes derived from activated astrocytes play a key role in the astrocyte-microglia interaction. miR-873a-5p, as one of the main components of these astrocyte-derived exosomes, attenuated microglia-mediated neuroinflammation and improved neurological deficits following TBI by inhibiting the NF-κB signalling pathway. These findings suggest a potential role for miR-873a-5p in treating traumatic brain injury.
Insights
Exosomes from activated astrocytes carry miR-873a-5p, which reduces neuroinflammation and improves outcomes after traumatic brain injury (TBI). This microRNA (miRNA) targets the NF-κB pathway, offering potential TBI therapeutic strategies.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Astrocytes and microglia interactions are crucial in traumatic brain injury (TBI) pathogenesis and repair.
- Exosomes mediate intercellular communication and are implicated in TBI.
- Understanding astrocyte-microglia communication via exosomes is vital for TBI treatment.
Purpose of the Study:
- To investigate the role of astrocyte-derived exosomes in TBI.
- To identify key microRNAs (miRNAs) within these exosomes.
- To elucidate the protective mechanism of miR-873a-5p in TBI.
Main Methods:
- Analyzed inflammatory factors and miR-873a-5p in TBI patient samples.
- Characterized astrocyte-derived exosomes using immunofluorescence, Western blot, and electron microscopy.
- Utilized TBI mouse and LPS-induced microglial models to assess exosome function.
Main Results:
- Astrocyte-derived exosomes promoted M2 microglial polarization post-TBI.
- miR-873a-5p was highly expressed in TBI exosomes and human brain tissue.
- miR-873a-5p inhibited M1 microglial polarization and inflammation by suppressing ERK and NF-κB signaling, improving neurological scores in mice.
Conclusions:
- miRNAs in astrocyte-derived exosomes are key mediators of astrocyte-microglia interactions in TBI.
- miR-873a-5p delivered via exosomes attenuates neuroinflammation and neurological deficits in TBI.
- miR-873a-5p shows promise as a therapeutic agent for traumatic brain injury.
