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Chronic Nicotine Exposure Systemically Alters MicroRNA Expression Profiles During Post-Embryonic Stages in Caenorhaoditis elegans

机译:慢性尼古丁暴露系统改变MicroRNA表达谱中Post-Embryonic阶段Caenorhaoditis线虫

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摘要

Tobacco smoking is associated with many diseases. Addiction is of the most notorious tobacco-related syndrome and is mainly attributed to nicotine. In this study, we employed Caenorhabditis elegons as a biological model to systemically investigate the effect of chronic nicotine exposure on microRNA (miRNA) expression profile and their regulated biochemicai pathways. Nicotine treatment (20 muM and 20 mM) was limited to the post-embryonic stage from LI to L4 (approx31 h) period after which worms were collected for genome-wide miRNA profiling. Our results show that nicotine significantly altered the expression patterns of 40 miRNAs. The effect was proportional to the nicotine dose and was expected to have an additive, more robust response. Based on pathway enrichment analyses coupled with nicotine-induced miRNA patterns, we inferred that miRNAs as a system mediates "regulatory hormesis", manifested in biphasic behavioral and physiological phenotypes. We proposed a model where nicotine addiction is mediated by miRNAs' regulation of fos-1 and is maintained by epigenetic factors. Thus, our study offers new insights for a better understanding of the sensitivity of early developmentai stages to nicotine.
机译:吸烟与许多疾病有关。上瘾是最臭名昭著的与烟草相关的综合征,是主要原因尼古丁。秀丽隠elegons作为生物模型系统调查慢性的影响尼古丁暴露在微rna (microRNA)表达式概要文件和他们的监管biochemicai通路。尼古丁的治疗(20妈妈和20毫米)是有限的从李post-embryonic阶段L4(approx31 h)时期之后,虫子收集全基因组microrna测定。结果表明,尼古丁显著改变40个microrna的表达模式。尼古丁的剂量成正比,预计将有添加剂,更健壮响应。再加上nicotine-induced microrna的模式,我们推断,microrna系统介导“监管毒物兴奋效应”,在两相的体现行为和生理表型。提出了一个模型,尼古丁上瘾由microrna的fos-1并监管由表观遗传因素。为更好的理解提供了新的见解早期developmentai阶段的敏感性尼古丁。

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