Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/95841
標題: Ochratoxin A induces ER stress and apoptosis in mesangial cells via a NADPH oxidase-derived reactive oxygen species-mediated calpain activation pathway
作者: 許美鈴
Sheu, Meei-Ling
Shen, Chin-Chang
Chen, Yuan-Siao
Chiang, Chih-Kang
關鍵字: ER stress
NADPH oxidase
apoptosis
mesangial cells
ochratoxin A
Animals
Apoptosis
Calcium Channel Blockers
Calpain
Cell Proliferation
Cells, Cultured
Endoplasmic Reticulum Stress
Mesangial Cells
Mice
NADPH Oxidases
Ochratoxins
Oxidation-Reduction
Oxidative Stress
Rats
Reactive Oxygen Species
Signal Transduction
出版社: ONCOTARGET
摘要: Ochratoxin A (OTA) contaminated food increases reactive oxygen species (ROS) production in glomerulus and causes glomerulopathy. The molecular mechanisms still remain uncertain. In this study, we used mouse and rat glomerular mesangial cells and delineate the signaling pathway behind the OTA-triggered cell apoptosis. OTA dose-dependently induced expression of ER stress markers including phospho-PERK, phospho-eIF2α, GRP78, GRP94, and CHOP. Apoptosis events including cleavage of caspase-12, caspase-7, and PARP are also observed. OTA activated oxidative stress and increased NADPH oxidase activity. NADPH oxidase inhibitor, apocynin, significantly attenuated OTA-induced cell apoptosis. Moreover, OTA markedly increased the calpain activity which significantly inhibited by apocynin. Transfection of calpain-siRNA effectively inhibited the OTA-increased ER stress-related protein expression. These findings suggest that OTA activated NADPH oxidase and calpain, induced ER stress and ROS production, and caused glomerular mesangial cells apoptosis which leads to glomerulopathy.
URI: http://hdl.handle.net/11455/95841
Appears in Collections:生物醫學研究所

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