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沙鼠短暂全脑缺血性脑缺血模型中αB-晶体蛋白表达的研究。

Study of αB-crystallin expression in Gerbil BCAO model of transient global cerebral ischemia.

机构信息

Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha 410011, China.

出版信息

Oxid Med Cell Longev. 2012;2012:945071. doi: 10.1155/2012/945071. Epub 2012 Oct 12.

DOI:10.1155/2012/945071
PMID:23097682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3477566/
Abstract

αB-crystallin (α-BC), the fifth member of mammalian small heat shock protein family (HspB5), is known to be expressed in many tissues and has a distinctive interaction with cytoskeleton components. In this study, we investigated that α-BC and microtubule-associated protein-2 (MAP-2), a neuron-specific cytoskeleton protein, were coexpressed in neurons of Gerbil cortex, while in subcortex Gerbil brains, we found that several MAP-2-negative glia cells also express α-BC. When subjected to 10-minute bilateral carotid artery occlusion (BCAO), an increment was observed in α-BC-positive cells after 6-hour reperfusion and peaked at around 7 days after. In the same circumstances, the number and the staining concentration of MAP-2 positive neurons significantly decreased immediately after 6-hour reperfusion, followed by a slow recovery, which is consistent with the increase of α-BC. Our results suggested that α-BC plays an important role in brain ischemia, providing the early protection of neurons by giving intracellular supports through the maintenance of cytoskeleton and extracellular supports through the protection of glia cells.

摘要

αB- 晶体蛋白(α-BC)是哺乳动物小热休克蛋白家族(HspB5)的第五个成员,已知在许多组织中表达,并与细胞骨架成分具有独特的相互作用。在这项研究中,我们发现在沙鼠大脑皮层的神经元中,α-BC 与微管相关蛋白-2(MAP-2)共表达,而在皮质下,我们发现一些 MAP-2 阴性神经胶质细胞也表达 α-BC。在进行 10 分钟双侧颈总动脉闭塞(BCAO)后,在 6 小时再灌注后观察到 α-BC 阳性细胞增加,并在 7 天左右达到峰值。在相同情况下,MAP-2 阳性神经元的数量和染色浓度在 6 小时再灌注后立即显著减少,随后缓慢恢复,这与 α-BC 的增加一致。我们的结果表明,α-BC 在脑缺血中发挥重要作用,通过维持细胞骨架为神经元提供早期保护,通过保护神经胶质细胞为神经元提供细胞外支持。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d8c/3477566/963d1b7e2f57/OXIMED2012-945071.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d8c/3477566/0798744a75bd/OXIMED2012-945071.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d8c/3477566/28e51f1a5923/OXIMED2012-945071.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d8c/3477566/963d1b7e2f57/OXIMED2012-945071.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d8c/3477566/0798744a75bd/OXIMED2012-945071.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d8c/3477566/28e51f1a5923/OXIMED2012-945071.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d8c/3477566/963d1b7e2f57/OXIMED2012-945071.003.jpg

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