Overexpression of ornithine decarboxylase suppresses thapsigargin-induced apoptosis.

doi:10.1007/s10059-010-0120-1

中山醫學大學機構典藏 CSMUIR > 醫學院 > 免疫學研究所 > 期刊論文 > Item 310902500/11706

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11706

Title:	Overexpression of ornithine decarboxylase suppresses thapsigargin-induced apoptosis.
Authors:	Hsieh, WC Hsu, PC Liao, YF Young, ST Wang, ZW Lin, CL Tsay, GJ Lee, H Hung, HC Liu, GY
Contributors:	中山醫學大學
Keywords:	endoplasmic reticulum (ER);mitochondrial membrane potential;ornithine decarboxylase (ODC);thapsigargin (TG)
Date:	2010
Issue Date:	2015-07-28T04:33:02Z (UTC)
ISSN:	1016-8478
Abstract:	Ornithine decarboxylase (ODC), the key enzyme of polyamine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC prevents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/endoplasmic reticulum (ER) Ca(2+) ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpression of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspase-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homologous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC preserved the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and down-stream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-mediated apoptotic pathway, induced by TG. Finally, overexpression of ODC maintains the protein and mRNA expression of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11706 http://dx.doi.org/10.1007/s10059-010-0120-1
Relation:	Mol Cells. 2010 Oct;30(4):311-8.
Appears in Collections:	[免疫學研究所] 期刊論文

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