Green Alastair D, Vasu Srividya, McClenaghan Neville H, Flatt Peter R
SAAD Centre for Pharmacy and Diabetes, University of Ulster, Cromore Road, Coleraine, BT52 1SA, Northern Ireland, UK.
Pflugers Arch. 2015 Oct;467(10):2219-28. doi: 10.1007/s00424-014-1681-1. Epub 2015 Jan 6.
We have studied the effects of cell communication on human beta cell function and resistance to cytotoxicity using the novel human insulin-secreting cell line 1.1B4 configured as monolayers and pseudoislets. Incubation with the incretin gut hormones GLP-1 and GIP caused dose-dependent stimulation of insulin secretion from 1.1B4 cell monolayers and pseudoislets. The secretory responses were 1.5-2.7-fold greater than monolayers. Cell viability (MTT), DNA damage (comet assay) and apoptosis (acridine orange/ethidium bromide staining) were investigated following 2-h exposure of 1.1B4 monolayers and pseudoislets to ninhydrin, H2O2, streptozotocin, glucose, palmitate or cocktails of proinflammatory cytokines. All agents tested decreased viability and increased DNA damage and apoptosis in both 1.1B4 monolayers and pseudoislets. However, pseudoislets exhibited significantly greater resistance to cytotoxicity (1.5-2.7-fold increases in LD50) and lower levels of DNA damage (1.3-3.4-fold differences in percentage tail DNA and olive tail moment) and apoptosis (1.3-1.5-fold difference) compared to monolayers. Measurement of gene expression by reverse-transcription, real-time PCR showed that genes involved with insulin secretion (INS, PDX1, PCSK1, PCSK2, GLP1R and GIPR), cell-cell communication (GJD2, GJA1 and CDH1) and antioxidant defence (SOD1, SOD2, GPX1 and CAT) were significantly upregulated in pseudoislets compared to monolayers, whilst the expression of proapoptotic genes (NOS2, MAPK8, MAPK10 and NFKB1) showed no significant differences. In summary, these data indicate cell-communication associated with three-dimensional islet architecture is important both for effective insulin secretion and for protection of human beta cells against cytotoxicity.
我们使用构建为单层和假胰岛的新型人胰岛素分泌细胞系1.1B4,研究了细胞通讯对人β细胞功能和细胞毒性抗性的影响。用肠促胰岛素胰高血糖素样肽-1(GLP-1)和葡萄糖依赖性促胰岛素多肽(GIP)孵育,可引起1.1B4细胞单层和假胰岛胰岛素分泌的剂量依赖性刺激。分泌反应比单层高1.5至2.7倍。在将1.1B4单层和假胰岛暴露于茚三酮、过氧化氢、链脲佐菌素、葡萄糖、棕榈酸酯或促炎细胞因子混合物2小时后,研究了细胞活力(MTT法)、DNA损伤(彗星试验)和细胞凋亡(吖啶橙/溴化乙锭染色)。所有测试试剂均降低了1.1B4单层和假胰岛的活力,增加了DNA损伤和细胞凋亡。然而,与单层相比,假胰岛对细胞毒性表现出显著更高的抗性(半数致死剂量增加1.5至2.7倍),DNA损伤水平更低(尾DNA百分比和橄榄尾矩差异为1.3至3.4倍),细胞凋亡水平更低(差异为1.3至1.5倍)。通过逆转录实时聚合酶链反应测量基因表达表明,与单层相比,假胰岛中与胰岛素分泌相关的基因(胰岛素基因、胰腺十二指肠同源盒1基因、前蛋白转化酶枯草杆菌蛋白酶/kexin 1型基因、前蛋白转化酶枯草杆菌蛋白酶/kexin 2型基因、GLP-1受体基因和GIP受体基因)、细胞间通讯相关基因(连接蛋白43基因、连接蛋白40基因和钙黏蛋白1基因)和抗氧化防御相关基因(超氧化物歧化酶1基因、超氧化物歧化酶2基因、谷胱甘肽过氧化物酶1基因和过氧化氢酶基因)显著上调,而促凋亡基因(一氧化氮合酶2基因、丝裂原活化蛋白激酶8基因、丝裂原活化蛋白激酶10基因和核因子κB1基因)的表达无显著差异。总之,这些数据表明与三维胰岛结构相关的细胞通讯对于有效的胰岛素分泌以及保护人β细胞免受细胞毒性都很重要。