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Implanting Glass Spinal Cord Windows in Adult Mice with Experimental Autoimmune Encephalomyelitis
Published on: December 21, 2013
Bone marrow mesenchymal stem cells to ameliorate experimental autoimmune encephalomyelitis via modifying expression
Dariush Haghmorad1,2, Ali Khaleghian3, Majid Eslami4
1Cancer Research Center, Semnan University of Medical Sciences, Semnan, Iran.
Introduction:
Clinical and experimental studies highlighted the significant therapeutic role of Mesenchymal stem cells (MSCs) in neurodegenerative diseases. MSCs possess potent immunomodulatory properties by releasing exosomes, which generate a suitable microenvironment. microRNAs (miRNAs), as one of several effective bioactive molecules of exosomes, influence cellular communication and activities in recipient cells. Recent studies revealed that miRNAs could control the progression of multiple sclerosis (MS) via differentiation and function of T helper cells (Th).
Methods:
Here, we investigated the therapeutic effects of syngeneic-derived BM-MSC in experimental autoimmune encephalomyelitis (EAE) mouse model of MS by evaluating expression profile of miRNAs, pro- and anti-inflammatory in serum and brain tissues. Three-time scheme groups (6th day, 6th & 12th days, and 12th day, of post-EAE induction) were applied to determine the therapeutic effects of intraperitoneally received 1*106 of BM-MSCs.
Results:
The expression levels of mature isoforms of miR-193, miR-146a, miR-155, miR-21, and miR-326 showed that BM-MSCs treatment attenuated the EAE clinical score and reduced clinical inflammation as well as demyelination. The improved neurological functional outcome associated with enhanced expression of miR-193 and miR-146a, but decreased expression levels of miR-155, miR-21, and miR-326 were followed by suppressing effects on Th1/Th17 immune responses (reduced levels of IFN-γand IL-17 cytokine expression) and induction of Treg cells, immunoregulatory responses (increase of IL-10, TGF-β, and IL-4) in treatment groups.
Conclusion:
Our findings suggest that BM-MSCs administration might change expression patterns of miRNAs and downstream interactions followed by immune system modulation. However, there is a need to carry out future human clinical trials and complementary experiments.
Insights
Mesenchymal stem cells (MSCs) show therapeutic potential for multiple sclerosis (MS) by modulating immune responses through exosomal microRNAs (miRNAs). MSC treatment in an MS mouse model improved neurological function and reduced inflammation by altering specific miRNA profiles.
Area of Science:
- Neuroimmunology
- Stem Cell Biology
- Molecular Medicine
Background:
- Mesenchymal stem cells (MSCs) are recognized for their therapeutic potential in neurodegenerative diseases, particularly multiple sclerosis (MS).
- MSCs exert immunomodulatory effects via exosomes, which contain bioactive molecules like microRNAs (miRNAs) that influence cellular communication.
- miRNAs play a crucial role in regulating T helper cell differentiation and function, impacting MS progression.
Purpose of the Study:
- To investigate the therapeutic effects of bone marrow-derived MSCs (BM-MSCs) in a mouse model of MS (experimental autoimmune encephalomyelitis - EAE).
- To analyze the expression profiles of specific miRNAs in serum and brain tissues following BM-MSC treatment.
- To correlate miRNA expression changes with immune response modulation and neurological recovery in EAE mice.
Main Methods:
- BM-MSCs were administered intraperitoneally to EAE mice at different time points post-induction.
- Serum and brain tissues were collected to assess the expression levels of key miRNAs (miR-193, miR-146a, miR-155, miR-21, miR-326).
- Pro- and anti-inflammatory markers, including T helper cell populations (Th1, Th17, Treg) and associated cytokines (IFN-γ, IL-17, IL-10, TGF-β, IL-4), were evaluated.
Main Results:
- BM-MSC treatment significantly attenuated EAE clinical scores, inflammation, and demyelination.
- Neurological functional outcomes improved, correlating with increased expression of miR-193 and miR-146a.
- Decreased expression of miR-155, miR-21, and miR-326 was observed, alongside suppressed Th1/Th17 responses and enhanced Treg cell induction.
Conclusions:
- BM-MSC administration modulates miRNA expression patterns, leading to downstream immune system regulation.
- These findings suggest a potential therapeutic mechanism for MSCs in MS through miRNA-mediated immune modulation.
- Further human clinical trials are warranted to validate these results and explore therapeutic applications.
