期刊
JOURNAL OF DIABETES RESEARCH
卷 2016, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2016/4692478
关键词
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资金
- National Natural Science Foundation of China [81370885]
- Postgraduate Scientific Innovation Project of Chong Qing Education Commission [CYB14097]
- Youth Project of Third Military Medical University [SWH2013QN02]
- Youth Doctor Diabetes Research of China International Medical Foundation [2015-N-08]
Apoptosis of islet beta cells is a primary pathogenic feature of type 2 diabetes, and ER stress and mitochondrial dysfunction play important roles in this process. Previous research has shown that prostate apoptosis response-4 (Par-4)/NF-kappa B induces cancer cell apoptosis through endoplasmic reticulum (ER) stress and mitochondrial dysfunction. However, the mechanism by which Par-4/NF-kappa B induces islet beta cell apoptosis remains unknown. We used a high glucose/palmitate intervention to mimic type 2 diabetes in vitro. We demonstrated that the high glucose/palmitate intervention induced the expression and secretion of Par-4. It also causes increased expression and activation of NF-kappa B, which induced NIT-1 cell apoptosis and dysfunction. Overexpression of Par-4 potentiates these effects, whereas downregulation of Par-4 attenuates them. Inhibition of NF-kappa B inhibited the Par-4-induced apoptosis. Furthermore, these effects occurred through the ER stress cell membrane and mitochondrial pathway of apoptosis. Our findings reveal a novel role for Par-4/NF-kappa B in islet beta cell apoptosis and type 2 diabetes.
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