High level expression of OSBPL11 is associated with atherosclerosis and Alzheimer's disease.

IF 4.5 2区 医学 Q2 CELL BIOLOGY
Huayu Zhang, Yanyu Chen, Qian Xu, Xuanshuang Wu, Naiqi He, Zhong Ren, Guixue Wang, Zhihan Tang, Qiong Xiang, Lushan Liu
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引用次数: 0

Abstract

With the global aging population, the incidence of aging-related diseases such as Alzheimer's disease (AD) and atherosclerosis (AS) is increasing. AS has also been identified as a key risk factor for AD. However, the conjoint molecular mechanisms driving these diseases remain unclear. This study first used bioinformatics analysis to analyze gene expression data in the cortex of AD patients and plaques of AS patients. We identified OSBPL11 as a gene whose expression co-increased under both conditions, and it is expressed in macrophages in AS patients and astrocytes in AD patients. Further validation was conducted through patient sample collection and an ApoE-/- mouse model. Strikingly, our findings suggest that OSBPL11 plays a role in the development of both AS and AD, and that there is increased co-localization of OSBPL11 with macrophages and astrocytes. This discovery offers new insights into the association between AS and AD and offers a new target for the treatment AS and AD.

OSBPL11的高水平表达与动脉粥样硬化和阿尔茨海默病有关。
随着全球人口老龄化,阿尔茨海默病(AD)、动脉粥样硬化(as)等老龄化相关疾病的发病率不断上升。AS也被认为是AD的一个关键危险因素。然而,导致这些疾病的联合分子机制仍不清楚。本研究首次采用生物信息学分析方法分析了AD患者皮层和AS患者斑块中的基因表达数据。我们发现OSBPL11是在两种情况下表达共同增加的基因,它在as患者的巨噬细胞和AD患者的星形胶质细胞中表达。通过患者样本收集和ApoE-/-小鼠模型进一步验证。引人注目的是,我们的研究结果表明OSBPL11在AS和AD的发展中都起作用,并且OSBPL11与巨噬细胞和星形胶质细胞的共定位增加。这一发现为AS和AD之间的关系提供了新的见解,并为治疗AS和AD提供了新的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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