ASK1 in Amyloid ß Peptide-Induced Cerebral Endothelial Cell Apoptosis

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TMUIR > College of Medicine > Department of Medicine > Department of Microbiology and Immunology > Periodical Article > Item 987654321/1054

Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/1054

Title:	ASK1 in Amyloid ß Peptide-Induced Cerebral Endothelial Cell Apoptosis
Authors:	陳玫潔 Hsu MJ;Hsu CY;Chen BC;Chen MC;Ou George;Lin CH
Contributors:	醫學系微生物與免疫學科
Date:	2007
Issue Date:	2009-08-14 10:37:43 (UTC+8)
Abstract:	A pathological hallmark of Alzheimer's disease is accumulation of amyloid-beta peptide (Abeta) in senile plaques. Abeta has also been implicated in vascular degeneration in cerebral amyloid angiopathy because of its cytotoxic effects on non-neuronal cells, including cerebral endothelial cells (CECs). We explore the role of apoptosis signal-regulating kinase 1 (ASK1) in Abeta-induced death in primary cultures of murine CECs. Abeta induced ASK1 dephosphorylation, which could be prevented by selective inhibition of protein phosphatase 2A (PP2A) but not PP2B. ASK1 dephosphorylation resulted in its dissociation from 14-3-3. ASK1, released from 14-3-3 inhibition, activated p38 mitogen-activated protein kinase (p38MAPK), leading to p53 phosphorylation. p53, a proapoptotic transcription factor, in turn transactivated the expression of Bax, a proapoptotic protein. Transfection with various dominant-negative mutants (DNs), including ASK1 DN and p38MAPK DN, suppressed Abeta-induced p38MAPK activation, p53 phosphorylation, and Bax upregulation and partially prevented CEC death. Bax knockdown using a bax small interfering RNA strategy also reduced Bax expression and subsequent CEC death. These results suggest that Abeta activates the ASK1-p38MAPK-p53-Bax cascade to cause CEC death in a PP2A-dependent manner.
Relation:	The Journal of Neuroscience.(27):5719-5729.
Data Type:	article
Appears in Collections:	[Department of Microbiology and Immunology] Periodical Article

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