A review of heat shock protein induction following cerebellar injury.

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.