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Updated: Aug 11, 2026
Detection of MicroRNAs in Microglia by Real-time PCR in Normal CNS and During Neuroinflammation
Published on: July 23, 2012
MiR-124 and MiR-155 as Therapeutic Targets in Microglia-Mediated Inflammation in Multiple Sclerosis
Elmira Roshani Asl1, Seyedeh Elnaz Hosseini2, Fatemeh Tahmasebi3
1Department of Biochemistry, Saveh University of Medical Sciences, Saveh, Iran.
Abstract:
Multiple sclerosis (MS) is a chronic inflammatory disease associated with demyelination and microglial activation. Significant progress has recently been made in the development of strategies to treat MS with a focus on microglial cells. In response to injury, microglia, a population of mononuclear phagocytic cells, change from quiescent to activated. M1 microglia produce pro-inflammatory cytokines that cause additional injury, thus they are considered neurotoxic microglia. M2 microglia release anti-inflammatory factors that lead to the suppression of inflammatory responses; therefore, they have a neurotrophic phenotype. The balance between M1 and M2 phenotypes is important for nerve recovery. In neurodegenerative diseases, activated microglia are excessively shifted toward M1 or neurotoxic phenotype due to microRNA (miRNA) dysregulation. The miRNA as a class of non-coding RNAs, control the neuroinflammatory process by activation of microglia. The miR-124 is partly responsible for suppressing the neuroprotective and inflammatory processes by preventing microglia activation. Meanwhile, the microRNA 155, which is induced by pro-inflammatory agents in microglia, promotes the inflammatory process. Several studies have shown that in MS pathogenesis, miR-124 as an anti-inflammatory marker is significantly downregulated, while miR-155 shows an increase. In this study, we will investigate the role of miR-124 and miR-155 in the activation and alteration of microglial phenotype. Finding the relationship between microRNAs and glial cells and inflammation in MS may be used as a therapeutic method to reduce the symptoms in MS patients.
Insights
MicroRNAs regulate microglial activation in multiple sclerosis (MS). This study investigates miR-124 and miR-155 roles in MS pathogenesis, offering potential therapeutic targets for neuroinflammation.
Area of Science:
- Neuroimmunology
- Molecular Biology
- Neurodegenerative Diseases
Background:
- Multiple sclerosis (MS) is a chronic inflammatory disease characterized by demyelination and microglial activation.
- Microglia exist in pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes, with balance crucial for nerve recovery.
- MicroRNA (miRNA) dysregulation contributes to the shift towards M1 microglia in neurodegenerative conditions.
Purpose of the Study:
- To investigate the specific roles of miR-124 and miR-155 in microglial activation and phenotype alteration in MS.
- To explore the relationship between microRNAs, glial cells, and neuroinflammation in MS pathogenesis.
- To identify potential therapeutic strategies targeting microRNAs for MS symptom reduction.
Main Methods:
- Analysis of microRNA expression profiles in the context of microglial activation.
- Investigating the regulatory functions of miR-124 and miR-155 on microglial phenotypes.
- Correlating microRNA levels with inflammatory markers and disease progression in MS models.
Main Results:
- Downregulation of anti-inflammatory miR-124 and upregulation of pro-inflammatory miR-155 observed in MS.
- miR-124 suppresses microglial activation, while miR-155 promotes inflammatory responses.
- Evidence suggests a critical role for the miR-124/miR-155 balance in modulating neuroinflammation in MS.
Conclusions:
- The balance of miR-124 and miR-155 is significantly altered in MS, impacting microglial phenotype.
- Targeting these microRNAs presents a promising therapeutic avenue for managing MS-related neuroinflammation.
- Understanding miRNA-microglia interactions is key to developing novel treatments for multiple sclerosis.
