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葡萄糖对INS-1细胞活性氧及PTEN表达的调控 被引量:2

Regulation of Glucose upon Reactive Oxygen Species and PTEN Expression in INS-1 Cells
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摘要 目的:研究葡萄糖刺激胰岛β细胞后,是否通过活性氧(ROS)调控第10号染色体缺失的磷酸酶与张力蛋白同源物基因(PTEN)表达而参与胰岛素分泌信号通路的调控。方法:用不同浓度葡萄糖和H2O2短时间干预胰岛细胞系(INS-1细胞),分别检测细胞分泌胰岛素、细胞内ROS浓度及PTENmRNA表达。结果:(1)随着刺激的葡萄糖、H2O2浓度升高,INS-1细胞内ROS浓度和分泌的胰岛素逐渐升高。(2)随着葡萄糖刺激加大或H2O2浓度逐渐升高,INS-1细胞内PTENmRNA表达先受到抑制,但当刺激浓度超过一定范围后,抑制作用消失。结论:葡萄糖可能通过刺激胰岛细胞内ROS生成,以低浓度ROS作为信号分子抑制PTEN表达,成为调控胰岛素分泌的机制之一。 Objective:To study effect of reactive oxygen species (ROS) ,induced from hyperglucose,on the expression of PTEN gene in INS-1 cell line. Methods:The cultured INS-1 cell line was exposed to different concentrations of glucose and H2O2 for a short time. Then,concentrations of secreted insulin,ROS and phosphatase and tensin homologue detetell on chromososme ten (PTEN) mRNA levels in cultured cells were detected. Results: Concentrations of ROS in INS-1 cells and secreted insulin in- creased along with increased glucose or H2O2 exposure. The PTEN mRNA expression decreased along with increased glucose or H2O2 exposure,but when glucose or H2 O2 were above a certain concentration, their inhibition on PTEN mRNA expression disappeared. Conclusion: Low ROS derived from glucose metabolism can inhibit the PTEN gene expression,which may be one of insulin secretion mechanisms in INS-1 cells induced by glucose stimulation.
出处 《中国临床医学》 2010年第1期18-21,共4页 Chinese Journal of Clinical Medicine
基金 上海市金山区卫生局课题基金(编号2005-3) 上海市青年基金课题(编号2007-70)
关键词 葡萄糖 活性氧 第10号染色体缺失的磷酸酶与张力蛋白同源物基因(PTEN) 胰岛素 Glucose Reactive oxygen species Phosphatase and tensin homologue deleted on chromosome ten Insulin
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  • 1Maechler P,Jornot L,Wollheim CB. Hydrogen peroxide alters rnitochondrial activation and insulin secretion in pancreatic beta cells [J]. Biol Chem,1999,274:27905-27913.
  • 2Janjic D,Maechler P,Wolheim CB, et al. Free radical modula tion of insulin release in INS-1 cells exposed to alloxan[J]. Biochem Pharmacol, 1999,57:639-648.
  • 3Ehelt H, Peschke D, Bromine HJ, et al. Influence of melatonin on free radical -induced changes in rat pancreatic beta-cells in vitro[J]. Pineal Res,2000,28:65-72.
  • 4Rhee SG,Kang SW,Jeong W. Intracellular messenger function of hydrogen peroxide and its regulation by peroxiredoxins [J]. Curr Opin Cell Biol,2005,17:185-189.
  • 5Pi JB,Bai YS,Zhang Q, et al. Reactive oxygen species as a signal in glucose-stimulated insulin secretion [J]. Diabetes,2007, 56(7):1783-1791.
  • 6Archer SL,WuXC,Thebaud B. O2 sensing in the humanductus arteriosus:redoxsensitive K^+ channels are regulated by mitochondria derived hydrogen peroxide [J]. Biol Chem,2004,385: 205-216.
  • 7Kraft R,Grimm C,Grosse K. Hydrogen peroxide and ADP-ribose induce TRPM2-mediated calcium influx and cation currents in microglia [J]. Physiol Cell Physiol,2004,286:129-137.
  • 8Krippelt Drews P,Haberland C,Fingerle J. Effects of H2O2 on membrane potential and [Ca^+]I of cultured rat arterial smooth muscle cells [J]. Biochem Biophys Res Commun. 1995,209: 139-145.
  • 9Myers MP, Pass I, Batty IH, et al. The lipid phosphatase activity of PTEN is critical for its tumor supressor function[J]. Proc Natl Acad Sci USA,1998,95:13513-13518.
  • 10Vazquez F,Ramaswamy S, Nakamura N, et al. Phosphorylation of the PTEN tail regulates protein stability and function. Mol [J]. Cell Biol,2000,20: 5010-5018.

同被引文献78

  • 1楼海亚 林开清 叶大风 等.子宫内膜癌组织中PTEN基因的研究.癌症,2005,26(6):63-63.
  • 2Yang W, Lu J, Weng J, et al. Prevalence of diabetes among men and women in China[J]. N Engl J Med, 2010, 362( 12): 1090-1101.
  • 3Lawlor MA,Alessi DR.PKB/Akt:a key mediator of cell proliferation, survival and insulin responses [ J ].Cell Sci,2001,114 ( 16 ) :2903 -2910.
  • 4Hanada M,Feng J, Hemmings BA.Structure,regulation and function of PKB/AKT--a major therapeutic target [J]. Biochim Biophys Acta, 2004, 1697( 1-2):3-16.
  • 5Inoguchi T,Li P,Umeda F,et al.High glucose level and free fatty acid stimulate reactive oxygen species production through protein kinase C- dependent activation of NAD(P)H oxidase in cultured vascular cells [ J ]. Diabetes,2000,49( 11 ): 1939-1945.
  • 6Ge QM,Dong Y,Su Q.Effects of glucose and advanced glycation end products on oxidative stress in MIN6 cells [ J ].Cell Mol Biol (Noisy-le- grand),2010,56(Suppl) :1231-1238.
  • 7Susztak K,Raff AC,Schiffer M, et al.Glucose induced reactive oxygen species cause apoptosis of podoeytes and p0docyte depletion at the onset of diabetic nephropathy[ J ].Diabetes,2006,55 ( 1 ):225-233.
  • 8Pi J,Bai Y,Zhang Q,et al.Reactive oxygen species as a signal in glucose- stimulated insulin secretion [J]. Diabetes, 2007,56(7):1783-1791.
  • 9Hohmeier H,Newgard C.Cell lines derived from pancreatic islets [ J ]. Mol Cell Endocrinol, 2004,228 ( 1-2 ): 121-128.
  • 10Ebeh H,Peschke D,Bromme HJ,et al.Influence of melatonin on free radical-induced changes in rat pancreatic beta-cells in vitro [ J ] .Pineal Res,2000,28 (2) :65 -72.

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