唾液酸对人胶质细胞系MiR-320a和Let-7e表达的影响

IF 1 Q4 NEUROSCIENCES
Negar Noorbakhsh, Hamid Galehdari, Mohammad Shafiei
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引用次数: 1

摘要

唾液酸在分子和细胞水平的各种关键生理事件和病理过程中起着关键作用。唾液酸浓度的变化在许多病理过程中都可以观察到;例如,一些可用的数据存在于评估唾液酸水平和神经退行性疾病的患病率。据推测,唾液酸可以在调节多种未发现的神经变性因子和下游靶标中发挥重要作用。基质金属蛋白酶9 (MMP9)是改变不同浓度唾液酸溶液暴露的因素之一。因此,我们旨在研究唾液酸溶液暴露对胶质细胞系miR-320a和let-7e作为两个上游因子表达模式的可能影响。方法:从伊朗巴斯德研究所制备人神经胶质细胞系,用添加10%胎牛血清(FBS)的dulbecco's modified eagle培养基(DMEM)培养。通过比色法测定唾液酸的IC50值,评估细胞代谢活性3-(4,5-二甲基噻唑-2-基(MTT)),并以300、500、1000 μg/mL唾液酸处理胶质细胞系24 h,研究唾液酸配体对miR-320a和let-7e表达模式的影响。从大约10×106胶质细胞中分离总RNA,并从每个样本中用于互补dna (cDNA)合成。miR-320a和let-7e的定量分析采用实时聚合酶链反应(real-time polymerase chain reaction, PCR),统计分析采用SPSS v. 21软件。结果:实时数据分析显示miR-320a和let-7e的表达显著升高(p)。结论:唾液酸在胶质细胞系中作为促炎因子调控miR-320a和let-7e可能存在连锁反应。重点:不同病理状态下唾液酸浓度不同。MicroRNAs在许多生物过程和人类疾病中发挥作用。miR-320a和let-7e表达水平在不同唾液酸浓度下显著升高。简单的语言总结:神经系统的炎症是由许多因素引起的。唾液酸是一种促进细胞炎症的炎症因子,尤其是在神经胶质细胞中。这就是为什么它可以作为模拟几种神经退行性疾病的有用模型,包括帕金森氏症和多发性硬化症。唾液酸浓度的变化在许多病理状态下都可以观察到,这可能是识别炎症过程的有用标记。本研究旨在检测不同浓度唾液酸对胶质细胞中两种非编码rna的影响。我们的研究表明,这两种microrna在对唾液酸产生反应时显著增加。我们认为这两个microrna参与了与唾液酸相关的神经炎症通路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Effect of Sialic Acid on MiR-320a and Let-7e Expression in Human Glial Cell Line.

The Effect of Sialic Acid on MiR-320a and Let-7e Expression in Human Glial Cell Line.

The Effect of Sialic Acid on MiR-320a and Let-7e Expression in Human Glial Cell Line.

The Effect of Sialic Acid on MiR-320a and Let-7e Expression in Human Glial Cell Line.

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.

Highlights: Differing in sialic acid concentration is seen in various pathological states.MicroRNAs play a role in numerous biological processes and human disorders.miR-320a and let-7e expression levels displayed a significant increase in different sialic acid concentrations.

Plain language summary: Inflammation in the nervous system occurs because of numerous factors. Sialic acid is an inflammatory factor that promotes cellular inflammation, particularly in the glial cells. That is why it could serve as a useful model for simulating several neurodegenerative diseases, including Parkinson's and Multiple sclerosis. Changes in sialic acid concentration are observed in many pathological states, which could be a useful marker for identifying the inflammatory process. The present study was carried out to examine the impact of different concentrations of sialic acid on two non-coding RNAs in glial cells. Our research shows that these two microRNAs greatly increased when responding to sialic acid. We suggest that these two microRNAs are contributed to the neuroinflammatory pathways related to sialic acid.

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来源期刊
CiteScore
2.60
自引率
0.00%
发文量
64
审稿时长
4 weeks
期刊介绍: BCN is an international multidisciplinary journal that publishes editorials, original full-length research articles, short communications, reviews, methodological papers, commentaries, perspectives and “news and reports” in the broad fields of developmental, molecular, cellular, system, computational, behavioral, cognitive, and clinical neuroscience. No area in the neural related sciences is excluded from consideration, although priority is given to studies that provide applied insights into the functioning of the nervous system. BCN aims to advance our understanding of organization and function of the nervous system in health and disease, thereby improving the diagnosis and treatment of neural-related disorders. Manuscripts submitted to BCN should describe novel results generated by experiments that were guided by clearly defined aims or hypotheses. BCN aims to provide serious ties in interdisciplinary communication, accessibility to a broad readership inside Iran and the region and also in all other international academic sites, effective peer review process, and independence from all possible non-scientific interests. BCN also tries to empower national, regional and international collaborative networks in the field of neuroscience in Iran, Middle East, Central Asia and North Africa and to be the voice of the Iranian and regional neuroscience community in the world of neuroscientists. In this way, the journal encourages submission of editorials, review papers, commentaries, methodological notes and perspectives that address this scope.
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