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脑微小RNA-122水平降低是易卒中自发性高血压大鼠脑血管疾病的早期标志物。

A Decrease of Brain MicroRNA-122 Level Is an Early Marker of Cerebrovascular Disease in the Stroke-Prone Spontaneously Hypertensive Rat.

作者信息

Stanzione Rosita, Bianchi Franca, Cotugno Maria, Marchitti Simona, Forte Maurizio, Busceti Carla, Ryskalin Larisa, Fornai Francesco, Volpe Massimo, Rubattu Speranza

机构信息

IRCCS Neuromed, Pozzilli, Isernia, Italy.

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.

出版信息

Oxid Med Cell Longev. 2017;2017:1206420. doi: 10.1155/2017/1206420. Epub 2017 Jun 18.

DOI:10.1155/2017/1206420
PMID:28751928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5494068/
Abstract

Based on preliminary evidence that highlights microRNA-122 as a contributing factor to stroke pathogenesis, we aimed at assessing its expression level, along with the presence of early signs of cerebrovascular disease, in the brain of stroke-prone spontaneously hypertensive rat (SHRSP), a suitable model of human disease that accelerates stroke occurrence under a high sodium/low potassium (Japanese-style) diet (JD). After one month of JD, before stroke occurrence, brain microRNA-122 level was significantly decreased in SHRSP as compared to the stroke-resistant SHR (SHRSR). At this time, levels of markers of oxidative stress and inflammation, as well as of endothelial integrity and function, apoptosis and necrosis were differently modulated in the brains of JD-fed SHRSP as compared to SHRSR, pointing to a significant activation of all deleterious mechanisms underlying subsequent stroke development in SHRSP. We also showed that miR-122 improved survival of rat endothelial cerebral cells upon stress stimuli (excess NaCl, hydrogen peroxide). Our data suggest that a decrease of brain microRNA-122 level is deleterious and can be considered as an early marker of stroke in the SHRSP. Understanding the mechanisms by which microRNA-122 protects vascular cells from stress stimuli may provide a useful approach to improve preventive and treatment strategies against stroke.

摘要

基于初步证据表明，微小RNA-122是中风发病机制的一个促成因素，我们旨在评估其在易患中风的自发性高血压大鼠（SHRSP）大脑中的表达水平，以及脑血管疾病早期迹象的存在情况。SHRSP是一种人类疾病的合适模型，在高钠/低钾（日式）饮食（JD）下会加速中风的发生。在JD饮食一个月后，中风发生前，与抗中风的SHR（SHRSR）相比，SHRSP大脑中的微小RNA-122水平显著降低。此时，与SHRSR相比，JD喂养的SHRSP大脑中氧化应激、炎症标志物以及内皮完整性和功能、凋亡和坏死的水平受到不同程度的调节，这表明SHRSP随后中风发展的所有有害机制均被显著激活。我们还表明，miR-122在应激刺激（过量NaCl、过氧化氢）下可提高大鼠脑内皮细胞的存活率。我们的数据表明，大脑微小RNA-122水平的降低是有害的，可被视为SHRSP中风的早期标志物。了解微小RNA-122保护血管细胞免受应激刺激的机制，可能为改进中风的预防和治疗策略提供有用的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/b09faa4ce978/OMCL2017-1206420.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/218d28cb08af/OMCL2017-1206420.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/8b76b7b5447a/OMCL2017-1206420.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/66dd95da2b4f/OMCL2017-1206420.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/747c222f3e03/OMCL2017-1206420.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/9288e8813f14/OMCL2017-1206420.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/6412a438f337/OMCL2017-1206420.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/b09faa4ce978/OMCL2017-1206420.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/218d28cb08af/OMCL2017-1206420.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/8b76b7b5447a/OMCL2017-1206420.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/66dd95da2b4f/OMCL2017-1206420.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/747c222f3e03/OMCL2017-1206420.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/9288e8813f14/OMCL2017-1206420.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/6412a438f337/OMCL2017-1206420.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce4/5494068/b09faa4ce978/OMCL2017-1206420.007.jpg

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