Cleaved caspase-3 expression after experimental stroke exhibits different phenotypes and is predominantly non-apoptotic

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• 作者：Daniel-Christoph Wagner^a ; ^{daniel-christoph.wagner@izi.fraunhofer.de} ; Ute Maria Riegelsberger^a ; Stefanie Michalk^a ; Wolfgang H&#xe4 ; rtig^b ; Alexander Kranz^a ; Johannes Boltze^a ; ^c
• 关键词：Brain ischemia ; Animal model ; Cell death ; Caspase-3 ; Immunohistochemistry ; SHR
• 刊名：Brain Research
• 出版年：2011
• 出版时间：24 March 2011
• 年：2011
• 卷：1381
• 期：Complete
• 页码：237-242
• 全文大小：1786 K

文摘

Cleaved caspase-3 (CC3) is well known as an executioner protease of apoptosis following brain ischemia. However, an increasing body of evidence suggests several non-apoptotic functions of CC3. To improve our understanding of the relation between cell death-related and non-adverse effects of postischemic caspase-3 activation, we examined the spatiotemporal distribution and identity of CC3-positive cells at days 2, 3 and 4 after permanent middle cerebral artery occlusion in rats. The lacking colocalization of CC3 and TUNEL staining indicated, that CC3 expression was predominantly non-apoptotic. Nuclear CC3 expression was frequently found to be colocalized with GFAP-positive astrocytes within the tissue adjacent to the infarct, whereas cytoplasmatic CC3 expression occurred solely in the lesion. Multiple fluorescence labeling revealed costaining of cytoplasmatic CC3 with markers directed against astrocytes, macrophages/microglia and supposedly pericytes. Our findings suggest that CC3 expression was predominantly associated with cellular responses to stroke such as reactive astrogliosis and the infiltration of macrophages.