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Original Paper

NADPH Oxidase 2-derived Reactive Oxygen Species are Involved in Dysfunction and Apoptosis of Pancreatic β-cells Induced by Low Density Lipoprotein

Li M.1 · Dou L.1,2 · Jiao J.1,2,3 · Lu Y.1,2 · Guo H.-B.1 · Man Y.1 · Wang S.1 · Li J.1,2 · These authors contributed equally to this work

Author affiliations

1The Key Laboratory of Geriatrics, Beijing Hospital & Beijing Institute of Geriatrics, Ministry of Health, Beijing;2Graduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing;3Department of Central Laboratory, General Hospital of Beijing Military Command, Beijing

Corresponding Author

Shu Wang and Jian Li, Beijing Institute of Geriatrics, Beijing Hospital, Ministry of Health No.1, Dahua Road, Dong Dan, Beijing 100730 (China) Tel.+8610-58115048(o), Fax +86 10 65237929 E-Mail lijian@bjhmoh.cn (J. Li), ws3704@yahoo.com.cn (S.Wang)

Related Articles for ""

Cell Physiol Biochem 2012;30:439-449

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Background: Increased levels of plasma cholesterol are a common feature of patient of type 2 diabetes. However, the links between elevated levels of low-density lipoprotein (LDL) and dysfunction of β-cells are still unclear. Methods: The apoE-/-mice were fed with a high-fat, cholesterol-rich diet for 8 weeks. Blood samples were collected from the mice for measurement of plasma glucose, lipids. The pancreas were embedded in OCT compound and frozen immediately in liquid nitrogen for further analysis. To examine the effects of LDL on β-cell function, insulin content, cell apoptosis and ROS production were measured in pancreatic islets of apoE-/-mice and mouse pancreatic β–cell line NIT-1. Relative cell signal pathways were determined by Western blot. Results: Decreased insulin content and increased apoptosis and ROS production were found in pancreatic islets of apoE-/-mice, accompanied by elevated plasma LDL. The ROS levels were significantly enhanced in NIT-1 cells exposed to LDL. Reduced insulin synthesis and glucose-stimulated insulin secretion and elevated apoptosis were reversed by suppression of NOX2 expression. Moreover, LDL induced dysfunction and apoptosis of pancreatic NIT-1 cells through JNK and p53 pathways, which were rescued by siRNA-mediated NOX2 reduction. Conclusions: NOX2-derived ROS may play a key role in LDL-induced dysfunction and apoptosis of pancreatic β-cells through JNK and p53 pathways.

© 2012 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: June 15, 2012
Published online: July 06, 2012
Issue release date: July 2012

Number of Print Pages: 11
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

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