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MicroRNA-7, synergizes with RORα, negatively controls the pathology of brain tissue inflammation
Dongxu Yue1,2, Juanjuan Zhao1,2, Huizi Chen1,2
1Special Key Laboratory of Gene Detection & Therapy of Guizhou Province, Zunyi, 563099, Guizhou, China.
Background:
Accumulating evidence has documented that microRNA-7 (miR-7) plays an important role in the pathology of various diseases. However, the potential role of miR-7 in brain tissue inflammation (BTI) remains unclear.
Methods:
We detected the expression of miR-7 in LPS-induced murine BTI model and observed the possible effects of miR-7 deficiency on the pathology of BTI. To elucidate the mechanism, the target gene of miR-7 was screened out by Gene chip assay and its potential roles in BTI were evaluated by Western blot, immunofluorescence, and RNAi assay, respectively.
Results:
MiR-7 was upregulated in brain tissue in BTI mice and its deficiency could significantly aggravate the pathology of brain tissue. Moreover, RORα, a new target molecule of miR-7, was upregulated in brain tissue from miR-7 deficiency BTI mice. Of note, downregulation of RORα could remarkably exacerbate the pathology of brain tissue and elevate the transduction of NF-κB and ERK1/2 signaling pathways in brain tissue from miR-7 deficiency BTI mice. Furthermore, RORα and miR-7 were dominantly co-expressed in neurons of BTI mice. Finally, RORα synergized with miR-7 to control the inflammatory reaction of neuronal cells in response to LPS stimulation.
Conclusions:
MiR-7 expression is upregulated in BTI model. Moreover, miR-7 synergizes with its target gene RORα to control the inflammation reaction of neurons, thereby orchestrating the pathology of BTI.
Insights
MicroRNA-7 (miR-7) is upregulated in brain tissue inflammation (BTI). It works with RORα to control neuronal inflammation, impacting BTI pathology.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- MicroRNA-7 (miR-7) is implicated in various disease pathologies.
- Its specific role in brain tissue inflammation (BTI) requires further investigation.
Purpose of the Study:
- To investigate the role and mechanism of miR-7 in a lipopolysaccharide (LPS)-induced murine BTI model.
- To identify miR-7 targets and their involvement in BTI pathogenesis.
Main Methods:
- Detection of miR-7 expression in LPS-induced BTI mice.
- Assessment of miR-7 deficiency effects on BTI pathology.
- Gene chip assay to identify miR-7 targets.
- Western blot, immunofluorescence, and RNAi assays to evaluate target gene roles.
Main Results:
- miR-7 expression was upregulated in BTI brain tissue.
- miR-7 deficiency exacerbated BTI pathology.
- RORα was identified as a miR-7 target, upregulated in miR-7 deficient BTI mice.
- RORα downregulation worsened BTI pathology and increased NF-κB and ERK1/2 signaling.
- miR-7 and RORα were co-expressed in neurons and synergistically controlled neuronal inflammatory responses.
Conclusions:
- miR-7 is upregulated in BTI and plays a protective role.
- miR-7, through its target RORα, regulates neuronal inflammation and orchestrates BTI pathology.
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