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Vol. 64 No. 4: Issue 4

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Up-regulation of receptor interaction protein 140 promotes glucolipotoxicity-induced damage in MIN6 cells

https://doi.org/10.14715/cmb/2018.64.4.7
Li Jun Xue
Department of Endocrinology, The second Clinical Medical college, Yangtze University, Jingzhou, Hubei, 434020, P.R. China
Qi Huang
Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, P.R. China
Jiao E Zeng
Department of Endocrinology, The second Clinical Medical college, Yangtze University, Jingzhou, Hubei, 434020, P.R. China
Hui Zhu
Department of Geratology, The General Hospital of The Yangtze River Shipping, Wuhan, Hubei, 430010, P.R. China
Cheng Yan Xu
Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, P.R. China

Corresponding Author(s) : Li Jun Xue

jzyyendoxjl@qq.com

Cellular and Molecular Biology, Vol. 64 No. 4: Issue 4

Abstract

The receptor interaction protein 140 (RIP140) cofactor is a key regulator of metabolic balance, but its function in glucose- and lipid-mediated damage in islet β cells is unknown and was investigated in this study. RIP140 expression and distribution was evaluated in MIN6 cells under high glucose and lipid conditions using real-time Polymerase Chain Reaction (PCR), western blotting and confocal laser scanning microscopy. Cells were separately treated with 500 μM palmitic acid and 25 mM glucose when RIP140 expression was upregulated or downregulated, and cell viability, apoptosis rate, the level of oxidative stress and insulin secretion was assessed, as was the expression of related genes. Increased glucose and palmitic acid elevated RIP140 expression and distribution in nuclei. Overexpression of RIP140 promoted apoptosis but inhibited cell viability in MIN6 cells, and basal insulin secretion and glucose-stimulated insulin secretion levels were altered following treatment with glucose and palmitic acid. In addition, oxidative stress was elevated, phosphorylated extracellular signal-regulated kinases 1/2 and uncoupling protein 2 messenger RNA (mRNA) abundance were increased, B-cell lymphoma-2 protein levels were decreased, and peroxisome proliferators activated receptor gamma co-activator 1 alpha, phosphoenolpyruvate carboxykinase , and pancreatic and duodenal homeobox-1 mRNA levels were downregulated. Furthermore, glucolipotoxicity-induced damage was reversed when RIP140 expression was downregulated by small interfering RNA (SiRNA). RIP140 promotes islet β cells damage caused by glucolipotoxicity.

Keywords

Receptor interaction protein 140 Islet β cell Glucolipotoxicity Oxidative damage Expression analysis.
Xue, L. J., Huang, Q., Zeng, J. E., Zhu, H., & Xu, C. Y. (2018). Up-regulation of receptor interaction protein 140 promotes glucolipotoxicity-induced damage in MIN6 cells. Cellular and Molecular Biology, 64(4), 39–45. https://doi.org/10.14715/cmb/2018.64.4.7
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