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小脑损伤后热休克蛋白诱导的综述。

A review of heat shock protein induction following cerebellar injury.

作者信息

Reynolds Laura P R, Allen Gary V

机构信息

Dalhousie University, Halifax, Canada.

出版信息

Cerebellum. 2003;2(3):171-7. doi: 10.1080/14734220310016114.

Abstract

Exposure of cells to stressful environments such as heat shock, ischemia, trauma and disease, induces the cellular expression of heat shock proteins (Hsps). Since the discovery of heat shock proteins in the early 1960s, efforts to understand their function in both stressed and non-stressed cells have remained the focus of a vast collection of researchers. Post-injury heat shock protein induction is believed to identify regions of reversible cell injury as well as contribute to repair and protective mechanisms following stress. With the role of cerebellum expanding to include a number of cognitive processes in addition to contributing to motor coordination, research contributions that further our understanding of cerebellar repair strategies following injury are significant. Following cellular stress, heat shock protein expression was observed in both neuronal and glial cell populations in the injured cerebellum. Specifically, Hsp27 expression was localized primarily in Purkinje cells and glial cells within the injured cerebellum, whereas Hsp72 induction was more prominent in the granule cell layer of the cerebellum. Thus, there appears to be a preferential expression of different families of heat shock proteins in different cell populations in the injured cerebellum. There are also distinct post-injury time frames of induction for each family of heat shock protein, emphasizing differences in cellular functional requirements for each family of heat shock protein. Hsp27 was expressed immediately following injury and continued up to 20 days post-injury whereas Hsp72 was expressed immediately following injury and disappeared by 4 days post-injury, suggesting the latter contributes to processes involved in the initial repair of injured cells. This review discusses heat shock protein induction patterns in both in vivo and in vitro cerebellar injury models and provides suggestions as to the functional role of heat shock proteins in the injured cerebellum.

摘要

将细胞暴露于热休克、缺血、创伤和疾病等应激环境中,会诱导细胞表达热休克蛋白(Hsps)。自20世纪60年代初发现热休克蛋白以来,了解它们在应激和非应激细胞中的功能一直是众多研究人员关注的焦点。损伤后热休克蛋白的诱导被认为可识别可逆性细胞损伤区域,并有助于应激后的修复和保护机制。随着小脑的作用扩展到除了促进运动协调外还包括许多认知过程,进一步加深我们对小脑损伤后修复策略理解的研究贡献意义重大。细胞应激后,在受伤小脑中的神经元和神经胶质细胞群体中均观察到热休克蛋白表达。具体而言,Hsp27表达主要定位于受伤小脑中的浦肯野细胞和神经胶质细胞,而Hsp72的诱导在小脑颗粒细胞层中更为突出。因此,在受伤小脑中不同细胞群体中似乎存在不同热休克蛋白家族的优先表达。每个热休克蛋白家族在损伤后的诱导时间框架也各不相同,这强调了每个热休克蛋白家族在细胞功能需求上的差异。Hsp27在损伤后立即表达,并持续到损伤后20天,而Hsp72在损伤后立即表达,并在损伤后4天消失,这表明后者有助于参与损伤细胞初始修复的过程。本综述讨论了体内和体外小脑损伤模型中的热休克蛋白诱导模式,并就热休克蛋白在受伤小脑中的功能作用提出了建议。

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