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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Investigation of cytocrom c oxidase gene subunits expression on the Multiple sclerosis
Naeimeh Safavizadeh1, Seyed Ali Rahmani, Mohamad Zaefizadeh
1Department of Biology, Ahar Branch, IAU university, Ahar, Iran.
Introduction:
Multiple sclerosis (MS) is an autoimmune inflamatory disease, which affects the (Central Nervous System) and leads to the destruction of myelin and atrophy of the axons. Genetic factors, in addition to environmental ones, seem to play a role in MS. Numerous studies have reported mitochondrial defects including a reduction in cytochrome c oxidase (COX) complex function related to the reduction of mitochondrial genes expression in the cortex tissue of patients with MS have been reported.
Materials And Methods:
This study aimed to assess COX5B and COX2 genes expression in MS patients and compare it with normal subjects. We determine expression levels of genes COX5B and COX2, and also gene reference ß-actine using real-time polymerase chain reaction (RT-PCR) method. Data were obtained and obtained and standardized with the gene reference and were analyzed using independent sample t-test with SPSS and Excel programs.
Result And Discussion:
The resultshowed COX5B gene expression reduced significant in MS patients compared to normal subjects (P < -0.05) whereas, there was no significant difference in the COX2 gene expression between normal subjects and patients. Thus, it can be claimed that down-regulation of mitochondrial electron transport chain genes supported the hypothesis that hypoxia-like tissue injury in MS may be due to mitochondrial genes, different expression impairment.
Insights
Multiple sclerosis (MS) patients show reduced expression of the COX5B gene, a key component of mitochondrial energy production. However, COX2 gene expression remained unchanged, suggesting specific mitochondrial gene dysregulation in MS.
Area of Science:
- Neuroscience
- Genetics
- Biochemistry
Background:
- Multiple sclerosis (MS) is an autoimmune disease affecting the central nervous system, causing myelin destruction and axonal atrophy.
- Both genetic and environmental factors contribute to MS pathogenesis.
- Mitochondrial dysfunction, including reduced cytochrome c oxidase (COX) complex activity and gene expression, is implicated in MS cortical tissue.
Purpose of the Study:
- To investigate the expression levels of COX5B and COX2 genes in the brain tissue of MS patients.
- To compare gene expression patterns between MS patients and healthy individuals.
- To explore the role of mitochondrial gene expression in MS pathology.
Main Methods:
- Gene expression analysis using real-time polymerase chain reaction (RT-PCR).
- Quantification of COX5B, COX2, and reference gene (ß-actin) expression levels.
- Statistical analysis using independent sample t-test.
Main Results:
- Significant reduction in COX5B gene expression was observed in MS patients compared to normal subjects (P < -0.05).
- No significant difference in COX2 gene expression was found between MS patients and normal subjects.
- These findings indicate differential regulation of mitochondrial electron transport chain genes in MS.
Conclusions:
- Down-regulation of COX5B suggests impaired mitochondrial electron transport chain function in MS.
- The results support the hypothesis that mitochondrial gene expression impairment contributes to hypoxia-like tissue injury in MS.
- Specific mitochondrial genes, like COX5B, may serve as potential biomarkers or therapeutic targets in MS.
