生物信息学分析确定大网膜蛋白在局灶性脑缺血损伤小鼠中的保护靶点

IF 2.5 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Wu Li , Jie Liu , Qi Zhang , Xiaojuan Ma , Jinwei Duan , Jiachen Wang , Ye Tian , Wenzhen Shi
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引用次数: 0

摘要

已知大网膜在缺血性中风中起保护作用。然而,其在IS发病机制中的调控网络和下游靶点目前尚未完全揭示。本研究建立大网膜过表达后光化学脑缺血模型。通过转录组分析获得8个关键差异表达基因(deg)。这些deg主要与激素分泌负调控、细胞磷酸离子稳态等途径有关。此外,在氧-葡萄糖剥夺(OGD)损伤的HT22细胞中,大网膜过表达后,预测基因3435 (Gm3435)、锚蛋白重复结构域53 (Ankrd53)、成纤维细胞生长因子23 (Fgf23) mRNA表达和Fgf23蛋白表达均下调。总之,我们的研究结果确定了IS后网膜调节的8个关键基因。在体外模型中进一步验证Gm3435、Ankrd53、Fgf23 mRNA表达和Fgf23蛋白表达与转录组学结果一致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bioinformatics analysis identifies the protective targets of omentin in mice with focal cerebral ischemia injury

Omentin is known to play a protective role in ischemic stroke. However, its regulatory networks and downstream targets in the pathogenesis of IS are incompletely revealed now. In this study, the model of photochemical brain ischemia was constructed after omentin over-expression. 8 key differentially expressed genes (DEGs) were obtained and analyzed by transcriptome analysis. These DEGs were mainly related to the negative regulation of hormone secretion, cellular phosphate ion homeostasis, and other pathways. Moreover, the mRNA expression of predicted gene 3435 (Gm3435), ankyrin repeat domain 53 (Ankrd53), fibroblast growth factor 23 (Fgf23) and the Fgf23 protein expression were down-regulated after omentin over-expression in HT22 cells injured by oxygen-glucose deprivation (OGD). In conclusion, our findings identified 8 key DEGs regulated by omentin after IS. In vitro models, the Gm3435, Ankrd53, Fgf23 mRNA expression and the Fgf23 protein expression were further verified to consistent with the transcriptomics results.

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来源期刊
Prostaglandins & other lipid mediators
Prostaglandins & other lipid mediators 生物-生化与分子生物学
CiteScore
5.80
自引率
3.40%
发文量
49
审稿时长
2 months
期刊介绍: Prostaglandins & Other Lipid Mediators is the original and foremost journal dealing with prostaglandins and related lipid mediator substances. It includes basic and clinical studies related to the pharmacology, physiology, pathology and biochemistry of lipid mediators. Prostaglandins & Other Lipid Mediators invites reports of original research, mini-reviews, reviews, and methods articles in the basic and clinical aspects of all areas of lipid mediator research: cell biology, developmental biology, genetics, molecular biology, chemistry, biochemistry, physiology, pharmacology, endocrinology, biology, the medical sciences, and epidemiology. Prostaglandins & Other Lipid Mediators also accepts proposals for special issue topics. The Editors will make every effort to advise authors of the decision on the submitted manuscript within 3-4 weeks of receipt.
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