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Updated: Jan 20, 2026
Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
Published on: September 9, 2022
MiR-125a-5p Regulates Vitamin D Receptor Expression in a Mouse Model of Experimental Autoimmune Encephalomyelitis
Han-Chun Long1,2, Rui Wu3, Chun-Feng Liu1,3
1Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, 215008, China.
Abstract:
Multiple sclerosis (MS) is a chronic and incurable autoimmune neurodegenerative disease of the central nervous system. Although the symptoms of MS can be managed by vitamin D3 treatment alone, this condition cannot be completely eradicated. Thus, there might be unknown factors capable of regulating the vitamin D receptor (VDR). Genome-wide analysis showed that miRNAs were associated with VDRs. We sought to determine the role and mechanism of action of miRNA-125a-5p and VDRs in a model of MS, mice with experimental autoimmune encephalomyelitis (EAE), which was induced by myelin oligodendrocyte glycoprotein 35-55 peptides. EAE mice showed decreased mean body weight but increased mean clinical scores compared with vehicle or control mice. And inflammatory infiltration was found in the lumbosacral spinal cord of EAE mice. In addition, VDR expression was significantly lower while the expression of miR-125a-5p was markedly higher in the spinal ventral horn of EAE mice than in vehicle or control mice. Importantly, activation of VDRs by paricalcitol or inhibition of miR-125a-5p by its antagomir markedly decreased the mean clinical scores in EAE mice. Interestingly, VDR and miR-125a-5p were co-localized in the same neurons of the ventral horn. More importantly, inhibition of miR-125a-5p remarkably blocked the decrease of VDRs in EAE mice. These results support a critical role for miR-125a-5p in modulating VDR activity in EAE and suggest potential novel therapeutic interventions.
Insights
MicroRNA-125a-5p regulates the vitamin D receptor (VDR) in multiple sclerosis (MS) models. Inhibiting this microRNA improves symptoms and VDR levels in experimental autoimmune encephalomyelitis (EAE), suggesting new therapeutic targets.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Multiple sclerosis (MS) is a chronic autoimmune neurodegenerative disease.
- Vitamin D receptor (VDR) activity is crucial for managing MS symptoms, but complete eradication remains elusive.
- MicroRNAs (miRNAs) have been implicated in VDR regulation.
Purpose of the Study:
- To investigate the role and mechanism of miRNA-125a-5p in regulating VDR in a mouse model of MS (experimental autoimmune encephalomyelitis - EAE).
- To explore potential therapeutic strategies targeting the miRNA-125a-5p/VDR pathway in EAE.
Main Methods:
- Induction of EAE in mice using myelin oligodendrocyte glycoprotein 35-55 peptides.
- Assessment of clinical scores, body weight, and spinal cord inflammation.
- Quantification of VDR and miRNA-125a-5p expression in spinal cord ventral horn.
- Treatment with VDR activator (paricalcitol) or miRNA-125a-5p inhibitor (antagomir).
Main Results:
- EAE mice exhibited increased clinical scores, decreased body weight, and spinal cord inflammation.
- VDR expression was reduced, while miRNA-125a-5p expression was elevated in the spinal ventral horn of EAE mice.
- VDR activation or miRNA-125a-5p inhibition significantly reduced EAE clinical scores.
- Inhibition of miRNA-125a-5p prevented the decrease in VDR expression in EAE mice.
Conclusions:
- MiRNA-125a-5p plays a critical role in modulating VDR activity in the context of EAE.
- The interaction between miRNA-125a-5p and VDR presents a potential novel therapeutic target for MS.
- Targeting miRNA-125a-5p may offer a new strategy for managing MS progression.
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