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脑外泌体中病理性鞘脂神经醇在克拉伯病小鼠模型中的分泌。

The Pathogenic Sphingolipid Psychosine is Secreted in Extracellular Vesicles in the Brain of a Mouse Model of Krabbe Disease.

机构信息

Department of Anatomy and Cell Biology, College of Medicine, 12247University of Illinois at Chicago, Chicago, IL, USA.

Department of Pharmaceutical Science, College of Pharmacy, 15481Oregon State University, Corvallis, OR, USA.

出版信息

ASN Neuro. 2022 Jan-Dec;14:17590914221087817. doi: 10.1177/17590914221087817.

Abstract

Psychosine exerts most of its toxic effects by altering membrane dynamics with increased shedding of extracellular vesicles (EVs). In this study, we discovered that a fraction of psychosine produced in the brain of the Twitcher mouse, a model for Krabbe disease, is associated with secreted EVs. We evaluated the effects of attenuating EV secretion in the Twitcher brain by depleting ceramide production with an inhibitor of neutral sphingomyelinase 2, GW4869. Twitcher mice treated with GW4869 had decreased overall EV levels, reduced EV-associated psychosine and unexpectedly, correlated with increased disease severity. Notably, characterization of well-established, neuroanatomic hallmarks of disease pathology, such as demyelination and inflammatory gliosis, remained essentially unaltered in the brains of GW4869-treated Twitcher mice compared to vehicle-treated Twitcher controls. Further analysis of Twitcher brain pathophysiology is required to understand the mechanism behind early-onset disease severity in GW4869-treated mice. The results herein demonstrate that some pathogenic lipids like psychosine may be secreted using EV pathways. Our results highlight the relevance of this secretory mechanism as a possible contributor to spreading pathogenic lipids in neurological lipidoses.

摘要

神经醇胺通过增加细胞外囊泡(EVs)的脱落来发挥其大部分毒性作用。在这项研究中,我们发现,震颤搐搦症(Krabbe 病的模型)小鼠大脑中产生的一部分神经醇胺与分泌的 EVs 有关。我们通过用神经鞘氨醇酶 2 的抑制剂 GW4869 耗尽神经酰胺的产生来评估减轻震颤搐搦症大脑中 EV 分泌的效果。用 GW4869 治疗的震颤搐搦症小鼠的总体 EV 水平降低,与 EV 相关的神经醇胺减少,出乎意料的是,与疾病严重程度增加相关。值得注意的是,与 vehicle-treated Twitcher 对照相比,GW4869 治疗的震颤搐搦症小鼠大脑中的疾病病理学的既定神经解剖学标志,如脱髓鞘和炎症性神经胶质增生,基本上没有改变。需要进一步分析震颤搐搦症大脑的病理生理学,以了解 GW4869 治疗的小鼠中早期疾病严重程度背后的机制。本文的结果表明,一些致病脂质,如神经醇胺,可能通过 EV 途径分泌。我们的结果强调了这种分泌机制的相关性,因为它可能是神经脂质病中传播致病脂质的一个可能因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aed0/8943320/12f79fbf65dc/10.1177_17590914221087817-fig1.jpg

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