Increased Mitochondrial DNA Copy Number and Oxidative Damage in Patients with Hashimoto's Thyroiditis.

BACKGROUND: The purpose of present study was to investigate mitochondrial DNA copy number (mtDNAcn) and mtDNA damage in peripheral blood of patients with Hashimoto's thyroiditis (HT) and healthy controls (HC). METHODS: The relative mtDNAcn and oxidative DNA damage in this case-control study were measured in peripheral blood of 50 patients with Hashimoto's thyroiditis and 50 healthy controls using quantitative real-time PCR. The study was conducted in Tehran University of Medical Sciences hospital, Tehran, Iran in 2018. RESULTS: HT patients had significantly higher mitochondrial DNA copy number and mitochondrial oxidative damage than the comparison group. CONCLUSION: These data suggest the possible involvement of mitochondria and oxidative stress in the pathophysiology of HT.

Analysis of Micro-RNA-144 Expression Profile in Patients with Multiple Sclerosis in Comparison with Healthy Individuals.

BACKGROUND: Etiology of multiple sclerosis is non-clarified. It seems that environmental factors impact epigenetic in this disease. Micro-RNAs (MIR) as epigenetic factors are one of the most important factors in non-genetically neurodegenerative diseases. It has been found MIR-144 plays a main role in the regulation of many processes in the central nervous system. Here, we aimed to investigation of MIR-144 expression alteration in Multiple sclerosis (MS) patients. METHODS: In this study 32 healthy and 32 MS patient's blood sample were analyzed by quantitative Real-Time PCR method and obtained data analyzed by REST 2009 software. RESULTS: Analysis of Real-Time PCR data revealed that miR-144 Increase significantly in MS patients compared to healthy controls. CONCLUSION: The increase of MIR-144 expression in MS patients is obvious. MIR-144 can be used as a biomarker of MS and help to early diagnosis and treatment of this disease.

Analysis of MicroRNA-18a Expression in Multiple Sclerosis Patients.

BACKGROUND: In multiple sclerosis (MS), the immune system acts against myelin lesions of the central nervous system, destroying neuronal fibers resulting in signal transmission disturbances in the nervous system. MicroRNAs play important roles in the post-transcriptional regulation of gene expression and in the regulation of disease activity and its response to treatment. The goal of this study was to determine the role of miR-18a-5p by comparing its expression in MS patients and healthy subjects. METHODS: RNA was isolated from blood samples of 32 MS patients and 32 healthy individuals, and miR-18a-5p expression was determined by real-time polymerase chain reaction (real-time PCR). RESULTS: miR-18a-5p expression was significantly less in MS patients than in healthy subjects. CONCLUSION: The reduction of miR-18a-5p expression may be via pathway signaling. Altered signaling plays an important role in MS pathogenesis and the miR-18a-5p expression profile in blood cells can be described as a prognostic biomarker and identifier of high-risk individuals in MS.

Quantification of mitochondrial DNA damage and copy number in circulating blood of patients with systemic sclerosis by a qPCR-based assay

Abstract Background: Although not fully understood, oxidative stress has been implicated in the pathogenesis of different autoimmune diseases such as systemic sclerosis. Accumulating evidence indicates that oxidative stress can induce mitochondrial DNA (mtDNA) damage and variations in mtDNA copy number (mtDNAcn). Objective: The aim of this study was to explore mtDNAcn and oxidative DNA damage byproducts in peripheral blood of patients with systemic sclerosis and healthy controls. Methods: Forty six patients with systemic sclerosis and forty nine healthy subjects were studied. Quantitative real-time PCR used to measure the relative mtDNAcn and the oxidative damage (oxidized purines) of each sample. Results: The mean mtDNAcn was lower in patients with systemic sclerosis than in healthy controls whereas the degree of mtDNA damage was significantly higher in cases as compared to controls. Moreover, there was a negative correlation between mtDNAcn and oxidative DNA damage. Study limitations: The lack of simultaneous analysis and quantification of DNA oxidative damage markers in serum or urine of patients with systemic sclerosis and healthy controls. Conclusion: These data suggest that alteration in mtDNAcn and increased oxidative DNA damage may be involved in the pathogenesis of systemic sclerosis.

Quantification of mitochondrial DNA damage and copy number in circulating blood of patients with systemic sclerosis by a qPCR-based assay.

BACKGROUND: Although not fully understood, oxidative stress has been implicated in the pathogenesis of different autoimmune diseases such as systemic sclerosis. Accumulating evidence indicates that oxidative stress can induce mitochondrial DNA (mtDNA) damage and variations in mtDNA copy number (mtDNAcn). OBJECTIVE: The aim of this study was to explore mtDNAcn and oxidative DNA damage byproducts in peripheral blood of patients with systemic sclerosis and healthy controls. METHODS: Forty six patients with systemic sclerosis and forty nine healthy subjects were studied. Quantitative real-time PCR used to measure the relative mtDNAcn and the oxidative damage (oxidized purines) of each sample. RESULTS: The mean mtDNAcn was lower in patients with systemic sclerosis than in healthy controls whereas the degree of mtDNA damage was significantly higher in cases as compared to controls. Moreover, there was a negative correlation between mtDNAcn and oxidative DNA damage. STUDY LIMITATIONS: The lack of simultaneous analysis and quantification of DNA oxidative damage markers in serum or urine of patients with systemic sclerosis and healthy controls. CONCLUSION: These data suggest that alteration in mtDNAcn and increased oxidative DNA damage may be involved in the pathogenesis of systemic sclerosis.