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KMID : 1161520150190010008
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Animal Cells and Systems
2015 Volume.19 No. 1 p.8 ~ p.15
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Coat protein I depletion-associated Golgi fragmentation in an Alzheimer's disease model
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Kim Mi-Jeong
Je A-Reum
Kim Hyo-Jeong
Huh Yang-Hoon
Kweon Hee-Seok
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Abstract
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The onset and progression of Alzheimer's disease (AD) is closely associated with amyloid β (Aβ) peptide-induced cytotoxicity and abnormal protein transportation caused by breakdown of endoplasmic reticulum (ER)?Golgi apparatus trafficking network. Although the fragmentation of Golgi apparatus has been reported in AD human patients and various AD model animals, the molecular mechanisms causing the morpho-functional impairments of Golgi apparatus during AD progression remain poorly understood. Thus, we investigated the ultrastructure of Golgi apparatus and coat protein I (COPI) expression in β-amyloid precursor protein/presenilin-1 double transgenic mouse and Aβ-stimulated BV-2 cell as an AD model using cryo-immunogold electron microscopy. In the neurons of the hippocampus of transgenic mouse and BV-2 cell, the cisternae of Golgi stacks were fragmented in difference with that of wild type mouse and cells. In addition, we further showed the COPI depletion in Golgi apparatus, which demonstrated the impairment of molecular integrities of Golgi apparatus. Taken together, our results provide insights into the Golgi apparatus-involved morphopathology of AD and we suggest that the Golgi fragmentation is caused by the depletion of COPI affecting the intra-Golgi transport through stimulation and accumulation of Aβ during AD development.
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KEYWORD
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Alzheimer's disease, amyloid β, coat protein I, Golgi apparatus, Golgi fragmentation
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