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首页> 外文期刊>Journal of Cellular Physiology >MALAT1 via microRNA-17 regulation of insulin transcription is involved in the dysfunction of pancreatic -cells induced by cigarette smoke extract
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MALAT1 via microRNA-17 regulation of insulin transcription is involved in the dysfunction of pancreatic -cells induced by cigarette smoke extract

机译：通过microRNA-17 MALAT1调节胰岛素转录的功能障碍肽引起的烟提取

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摘要

Cigarettes contain various chemicals with the potential to influence metabolic health. Exposure to cigarette smoke causes a dysfunction in pancreatic -cells and impairs insulin production. However, the mechanisms for cigarette smoke-induced reduction of insulin remain largely unclear. Data from 558 patients with diabetes showed that, with smoking pack-years, homeostatic model assessment (HOMA)- (a method for assessing -cell function) decreased and that HOMA of insulin resistance increased. For -cells (MIN6), cigarette smoke extract (CSE) increased the levels of thioredoxin-interacting protein (TXNIP) and the long noncoding (lnc)RNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), and downregulated the levels of the transcription factor, mafA, and microRNA (miR)-17. MALAT1, one of four lncRNAs predicted to regulate miR-17, was knocked down by small interfering RNA (siRNA). For these cells, an miR-17 mimic inhibited TXNIP and enhanced the production of insulin. Knockdown of MALAT1 induced an increase in miR-17, which suppressed TXNIP and promoted the production of insulin. In the sera of patients with diabetes who smoked, there were higher MALAT1 levels and lower miR-17 levels than in the sera of nonsmokers. Thus, CSE inhibits insulin production by upregulating TXNIP via MALAT1-mediated downregulation of miR-17, which provides an understanding of the processes involved in the reduced -cells function caused by cigarette smoke.
机译：香烟含有各种化学物质的可能影响代谢健康。吸烟会导致功能障碍肽和损害胰岛素生产。然而,香烟的机制减少烟雾诱发胰岛素仍很大程度上不清楚。显示,与吸烟久,自我平衡的模型评估(HOMA)——(一种评估的方法细胞功能),HOMA下降胰岛素抵抗增加。香烟烟雾提取物(CSE)增加了水平的thioredoxin-interacting蛋白(TXNIP)和长非编码RNA(信号),肺腺癌转移相关记录1 (MALAT1),表达下调转录因子的水平,mafA,微rna (miR) -17。预测控制mir - 17,被撞倒了小核RNA)。一个mir - 17模仿抑制TXNIP和增强生产胰岛素。诱导mir - 17的增加,抑制TXNIP和促进胰岛素的生产。糖尿病患者的血清,抽有MALAT1水平较高和较低的mir - 17比不吸烟者的血清水平。抑制胰岛素生产移植TXNIP通过以上的差别MALAT1-mediated对这些mir - 17,它提供了一个理解的过程参与肽功能降低所致香烟烟雾。

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