NDRG2 is highly expressed in pancreatic β cells and involved in protection against lipotoxicity
NDRG2 is highly expressed in pancreatic β cells and involved in protection against lipotoxicity
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DOI：
10.1007/s00018-010-0258-1
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发表时间：
2010-04-01
影响因子：
8
通讯作者：
Yao, Libo
中科院分区：
文献类型：
--
作者：
Shen, Lan;Liu, Xuewu;Yao, Libo
N-myc下游调节基因2（NDRG 2）参与细胞分化和凋亡，但其在胰腺中的功能仍有待确定。在此，我们研究NDRG 2在内分泌胰腺中的表达和功能。NDRG 2免疫反应主要定位于胰腺β细胞的胞浆中。当β-TC 3细胞长期暴露于高水平的游离脂肪酸（FFA）时，细胞活力受损，Akt和NDRG 2磷酸化降低。NDRG 2是蛋白激酶Akt的潜在底物。组成性激活Akt的过表达增强NDRG 2磷酸化并消除FFA诱导的β-TC 3细胞凋亡，而NDRG 2敲低减弱Akt介导的β细胞对脂肪酸触发的凋亡的保护。总的来说，这些数据表明NDRG 2作为胰腺β细胞中的关键分子，并参与Akt介导的β细胞抗脂毒性的保护。
The N-myc downstream-regulated gene 2 (NDRG2) is involved in cell differentiation and apoptosis, but its function in the pancreas remains to be established. Herein we examine the expression and function of NDRG2 in the endocrine pancreas. NDRG2 immunoreactivity was localized mainly in the cytoplasm of pancreatic beta cells. When beta-TC3 cells were exposed chronically to high levels of free fatty acid (FFA), cell viability was impaired, and Akt and NDRG2 phosphorylation were reduced. NDRG2 is a potential substrate of protein kinase Akt. Overexpression of constitutively active Akt enhanced NDRG2 phosphorylation and abolished the apoptosis induced by FFA in beta-TC3 cells, whereas NDRG2 knock-down attenuated Akt-mediated protection of beta cells against fatty acid-triggered apoptosis. Collectively, these data indicate that NDRG2 acts as a key molecule in pancreatic beta cells and is involved in the Akt-mediated protection of beta cells against lipotoxicity.