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Showing 4 results for Microrna

Melika Abrishami, Mostafa Rezaei-Tavirani,
Volume 0, Issue 0 (3-2018)
Abstract

Introduction: Multiple sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system. The diagnosis and monitoring of MS progression is challenging because of its complex pathogenesis and the lack of specific biomarkers. Introducing related microRANs and associated proteins with MS is aim of this study. 
Methods: MS-related miRNA data of 4 peripheral blood profiles from relapsing-remitting MS (RRMS) patients and 8 healthy controls were extracted from the GEO database. Their related proteins were analyzed using bioinformatics methods, such as protein-protein interaction (PPI) network and action map.
Results: Numbers of 18 differentially microRNA were detected which discriminate the patient samples from controls. The 31 related proteins were identified and assessed via PPI network analysis and action map evaluation.
Conclusion: In conclusion, a protein panel of NCL, NOP58, SNRNP70, U2AF2, YBX1, PRPF8, BOP1, and PIK3K as the crucial individuals which are associated with MS was suggested for further investigation.

Mohsen Sedighi, Tourandokht Baluchnejadmojarad, Soudabeh Fallah, Nariman Moradi, Siamak Afshin-Majd, Mehrdad Roghani,
Volume 11, Issue 3 (5-2020)
Abstract

Introduction: Klotho and dipeptidyl peptidase-4 (DPP4) are two proteins that modulate inflammatory pathways. We investigated the association between circulating klotho and DPP4 activity and their relationship with inflammatory cytokines, miR-29a, and miR-195 in Alzheimer disease (AD).
Methods: This study was conducted on 16 AD patients and 16 healthy age-matched controls. Plasma levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β, interleukin-6 (IL-6), klotho, and DPP4 were measured by enzyme-linked immunosorbent assay. Plasma expression of miR-29a and miR-195 were also measured and compared by a real-time polymerase chain reaction.
Results: There was a significant increase in TNF-α (p=0.006), IL-1β (p=0.012), and IL-6 (p=0.012) levels in the AD subjects compared with controls. Also, we found a decrease in plasma levels of klotho and an increase in plasma levels of DPP4 in the AD group that was not significant compared with the controls. Lower expression of miR-29a (P=0.009) and higher expression of miR-195 (P=0.003) were observed in the AD group that was significant than controls. Further analysis showed a negative correlation between klotho and plasma levels of IL-6 (r=-0.58, p=0.01). Also, there was a positive correlation between plasma DPP4 activity and TNF-α levels (r=0.50, P=0.04) and IL-1β (r=0.62, P=0.01). Likewise, plasma klotho concentration showed a negative correlation with the age of AD subjects (r=-0.56, P=0.02).
Conclusion: TNF-α, IL-1β, and IL-6 are involved in AD pathophysiology, and dysregulation of DPP4 and klotho may be associated with the inflammatory response of AD. Down-regulation of miR-29a and up-regulation of miR‑195 indicated the role of miRNAs in the AD process.
Negar Noorbakhsh, Hamid Galehdari, Mohammad Shafiei,
Volume 13, Issue 3 (5-2022)
Abstract

Introduction: Sialic acid is pivotal in various critical physiological events at molecular and cellular levels and pathological processes. Changes in sialic acid concentration are observed in many pathological processes; for example, some available data exist on the evaluated level of sialic acid and neurodegenerative prevalence. Presumably, sialic acid can play a significant role in regulating a diverse range of uncovered neurodegeneration factors and downstream targets. matrix metalloproteinases 9 (MMP9) is one factor that changes the exposure of different concentrations of sialic acid solution. Hence, we aimed to examine the possible effect of sialic acid solution exposure on the glial cell line in the expression patterns of miR-320a and let-7e as two upstream factors. 
Methods: Human glial cell line was prepared from the Pasteur Institute of Iran and cultured in a dulbecco’s modified eagle medium (DMEM) with 10% fetal bovine serum (FBS). The IC50 value of sialic acid was obtained by colorimetric assay for assessing cell metabolic activity 3-(4,5-Dimethylthiazol-2-yl (MTT), and the glial cell line was treated with sialic acid in 300, 500, 1000 µg/mL for 24 h to investigate the effect of the sialic acid ligand on the expression pattern of the miR-320a and let-7e. Total RNA was isolated from approximately 10×106 glial cells and was used from each sample for complementary dna (cDNA) synthesis. For quantitative analysis of miR-320a and let-7e, we used real-time polymerase chain reaction (PCR), and for statistical analysis, the SPSS v. 21 software was applied. 
Results: Analyzing the real-time data revealed that the expression of miR-320a and let-7e was significantly increased (P<0.0001) in 300, 500, and 1000 µg/mL treated glial cells by sialic acid compared to the control group. 
Conclusion: A possible linkage of sialic acid on miR-320a and let-7e regulation was observed in the glial cell line as proinflammatory factors in the inflammation pathway.

Dr Sanaz Mohammadi, Dr Salma Ahmadlou, Dr Leila Dargahi, Dr Mohammad Ismail Zibaii, Dr Pouria Ghasemi, Dr Afsaneh Asgari Taei, Dr Andisheh Balouchi, Dr Mohammad Reza Bigdeli,
Volume 15, Issue 6 (11-2024)
Abstract

Introduction: The developing and promising optogenetic stimulation method can aid functional recovery by carefully regulating neuronal activity in brain circuits damaged by a stroke lesion. This investigation assesses the potential pretreatment effects of optogenetic stimulation on an ischemic stroke animal model. 
Methods: Lentiviruses containing pLenti-CaMKIIa-hChR2 (H134R)-mCherry-WPRE were administered to adult male Wistar rats. It was injected into the right striatum for this purpose. Twenty-six days after the virus injection, the animals were exposed to blue laser light for six days in a row for 30 minutes at a time. Twenty-four hours after the final light stimulation, the transient middle cerebral artery occlusion (tMCAO) was done. One day after reperfusion, the neurological processes and the size of the brain infarcts in ischemic rats were evaluated. The transcript levels of microRNAs 21 and 124a—epigenetic indicators for neuroprotection and neurogenesis—were also assessed in the striatum and hippocampus.
Results: Our findings suggested that pretreatment with glutamatergic striatum optogenetic stimulation could reduce neurological impairments in rats and boost neuronal survival in both striatum and hippocampal regions. Also, the expression of microRNA-21 (miR-21) in the striatum was significantly increased in rats that had been optogenetically stimulated. Additionally, miR-124a expression was elevated in both regions in rats given tMCAO, and pretreatment with optical stimulations may considerably lower its expression in the hippocampus.
Conclusion: According to our findings, optogenetic stimulation pretreatment of the striatum positively affects stroke recovery. The effect is partially mediated by altering miRNAs involved in neurogenesis and subsequently activating its downstream signaling cascade.


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