期刊文献+

MicroRNA-29抑制胰岛素刺激的大鼠L6细胞葡萄糖吸收 被引量:4

MicroRNA-29 suppresses glucose uptake stimulated by insulin in L6 myotube cells
下载PDF
导出
摘要 目的研究microRNA-29(miR-29)在糖尿病模型大鼠(GK)骨骼肌组织中的表达,并探讨其对大鼠骨骼肌细胞L6葡萄糖吸收的影响。方法利用real-time PCR方法检测miR-29家族,miR-29a、miR-29b及miR-29c在GK大鼠骨骼肌组织中的表达特征。L6骨骼肌细胞诱导分化为肌管细胞,经葡萄糖与胰岛素处理后,利用real-time PCR与Northern blot分析miR-29家族的表达情况。选择腺病毒表达系统在L6分化的肌管细胞中过表达或抑制内源miR-29的功能,利用葡萄糖吸收实验检测胰岛素刺激的葡萄糖吸收情况。结果 miR-29a、miR-29b及miR-29c在GK大鼠骨骼肌组织中表达上调。L6分化的肌管细胞经葡萄糖与胰岛素处理,miR-29b和miR-29c的表达上调,而miR-29a表达无明显变化。在L6分化的肌管细胞中过表达miR-29可以明显抑制胰岛素刺激的葡萄糖吸收。结论miR-29参与了GK大鼠骨骼肌细胞葡萄糖耐受及胰岛素抵抗的产生,抑制其表达可能是治疗Ⅱ型糖尿病的一种新策略。 Objective To evaluate the expression profile of miR-29 family in skeleten muscle of GK rats and to fur- ther probe the function of miR-29 family in glucose uptake in L6 cells induced by insulin. Methods The expres- sion of miR-29 family was detected by RT-PCR. miR-29 level in L6 cells treated by glucose and insulin was meas- ured by using real-time PCR and Northern Blot. Gain or loss of function of miR-29 was achieved by a recombinant adenovirus system and the effect of miR-29 on insulin resistance was measured by insulin-induced glucose uptake assay. Results miR-29a, miR-29b, and miR-29c expression was upregulated in the skeletal muscle of GK rats and miR-29b and miR-29c expression levels were elevated in L6 cells treated by glucose and insulin. Moreover, enforced expression of miR-29 significantly suppressed insulin-induced glucose uptake in L6 cells and loss-of-func- tion of miR-29 by using Ad-sp-miR-29 led to an increase of glucose uptake. Conclusions miR-29 family is involved in the glucose tolerance and insulin resistance of GK rats and targeting miR - 2 9 maybe provide a novel strategy for the treatment of type Ⅱdiabetes.
出处 《基础医学与临床》 CSCD 北大核心 2013年第5期562-566,共5页 Basic and Clinical Medicine
基金 国家自然科学基金青年科学基金(81100608)
关键词 microRNA-29 Ⅱ型糖尿病 葡萄糖耐受 胰岛素抵抗 microRNA-29, Type Ⅱ diabetes, glucose tolerance, insulin resistance
  • 相关文献

参考文献12

  • 1Knowler WC, Fowler SE, Hamman RF, et al. 10-year fol- low-up of diabetes incidence and weight loss in the Diabetes Prevention Program .Outcomes Study [ J ]. Lancet, 2009, 374 : 1677 - 1686.
  • 2Nathan DM, Buse JB, Davidson MB, et al. Medical man- agement of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy: a consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes[ J]. Diabetes Care, 2009, 32 : 193 - 203.
  • 3Homstein E, Mansfield J H, Yekta S, et al. The microR- NA miR-196 acts upstream of Hoxb8 and Shh in limb devel- opment[ J]. Nature, 2005, 438:671 -674.
  • 4于岚,刘卫,陈松森,何小东,刘长征.MiR-21通过抑制RECK表达促进胆管癌细胞QBC939的侵袭[J].基础医学与临床,2012,32(5):510-515. 被引量:4
  • 5Yang C, Wang C, Chen X, et al. Identification of seven serum microRNAs from a genome-wide serum microRNA ex- pression profile as potential noninvasive biomarkers for ma- lignant astrocytomas[J]. Int J Cancer, 2013, 132:116 - 127.
  • 6He A, Zhu L, Gupta N, et al. Overexpression of micro ri- bonucleic acid 29, highly up-regulated in diabetic rats, leads to insulin resistance in 3T3-L1 adipocytes [ J ]. Mol Endocrinol, 2007, 21 : 2785 - 2794.
  • 7Onishi S, Takemoto M, Ishikawa T, et al. Japanese diabet- ic patients with Wemer syndrome exhibit high incidence of cancer[J]. Acta Diabetol, 2012, 49:259-260.
  • 8Lawson SK, Dobrikova EY, Shveygert M, et al. p38alpha mitogen-aetivated protein kinase depletion and repression of signal transduction to translation machinery by miR-124 and -128 in neurons[J]. Mol Cell Biol, 2013, 33:127 -135.
  • 9Ambros V. The functions of animal microRNAs [ J ]. Na- ture, 2004, 431 : 350 -355.
  • 10Zhang X, Zhao X, Fiskus W, et al. Coordinated silencing of MYC-mediated miR-29 by HDAC3 and EZH2 as a ther- apeutic target of histone modification in aggressive B-Cell lymphomas[J]. Cancer Cell, 2012, 22:506-523.

二级参考文献13

  • 1Friman S.Cholangiocarcinoma current treatment options[J].Scand J Surg,2011,100:30-34.
  • 2Charbel H,Al Kawas FH.Cholangiocarcinoma epidemiolo-gy risk factors pathogenesis and diagnosis[J].Curr Gastro-enterol Rep,2011,13:182-187.
  • 3Isa T,Tomita S,Nakachi A,et al.Analysis of microsatel-lite instability,K-ras gene mutation and p53 protein over-expression in intrahepatic cholangiocarcinoma[J].Hepato-gastroenterology,2002,49:604-608.
  • 4Xu L,Hausmann M,Dietmaier W,et al.Expression ofgrowth factor receptors and targeting of EGFR in cholangio-carcinoma cell lines[J].BMC Cancer,2010,10:302.
  • 5Thuwajit P,Chawengrattanachot W,Thuwajit C,et al.In-creased TFF1 trefoil protein expression in Opisthorchisviverrini-associated cholangiocarcinoma is important for in-vasive promotion[J].Hepatol Res,2007,37:295-304.
  • 6Jinawath A,Akiyama Y,Yuasa Y,et al.Expression ofphosphorylated ERK1/2 and homeodomain protein CDX2in cholangiocarcinoma[J].J Cancer Res Clin Oncol,2006,132:805-810.
  • 7Ambros V.The functions of animal microRNAs[J].Na-ture,2004,431:350-355.
  • 8Meng F,Henson R,Wehbe-Janek H,et al.MicroRNA-21regulates expression of the PTEN tumor suppressor gene inhuman hepatocellular cancer[J].Gastroenterology,2007,133:647-658.
  • 9Gabriely G,Wurdinger T,Kesari S,et al.MicroRNA 21promotes glioma invasion by targeting matrix metalloprotei-nase regulators[J].Mol Cell Biol,2008,28:5369-5380.
  • 10Liu C,Yu J,Yu S,et al.MicroRNA-21 acts as an oncomirthrough multiple targets in human hepatocellular carcinoma[J].J Hepatol,2010,53:98-107.

共引文献3

同被引文献54

  • 1陈琴,黄铭涵,张在保,郑行春.microRNA-503在糖尿病大鼠心肌梗死后血管新生过程中的变化[J].中国动脉硬化杂志,2015,23(3):261-265. 被引量:4
  • 2Gray SP,Cooper ME.Alleviating the burden of diabetic nephropathy[J].Nat Rev Nephrol,2011,7:71-73.
  • 3Argyropoulos C,Wang K,McClarty S,et al.Urinary microRNA profiling in the Nephropathy of Type1 Diabetes[J].PloS ONE,2013,8:e54662.doi:10.1371/journal.pone.0054662.
  • 4Kato M,Arce L,Wang M,et al.microRNA circuit mediates transforming growth factor beta1 autoregulation in renal glomerular mesangial cells[J].Kidney Int,2011,80:358-368.
  • 5Long J,Wang Y,Wang W,et al.MicroRNA-29c is a signature microRNA under high glucose conditions that targets Sprouty homolog 1,and its in vivo knockdown prevents progression of diabetic nephropathy[J].J Biol Chem,2011,286:11837-11848.
  • 6Putta S,Lanting LD,Sun GD,et al.Inhibiting MicroRNA-192 Ameliorates Renal Fibrosis in Diabetic Nephropathy[J].J Am Soc Nephrol,2012,23:458-469.
  • 7Yang Y,Xiao L,Li J,et al.Urine miRNAs:Potential biomarkers for monitoring progression of early stages of diabetic nephropathy[J].Med Hypotheses,2013,81:274-278.
  • 8Dey N,Das F,Mariappan MM,et al.MicroRNA-21 orchestrates high glucose-induced signals to TOR complex1,resulting in renal cell pathology in diabetes[J].J Biol Chem,2011,286:25586-25603.
  • 9Zarjou A,Yang S,Abraham E,et al.Identification of a microRNA signature in renal fibrosis:role of miR-21[J].Am J Physiol Renal Physiol,2011,301:793-801.
  • 10Wang B,Koh P,Winbanks C,et al.miR-200a prevents renal fibrogenesis through repression of TGF-beta2 expression[J].Diabetes,2011,60:280-287.

引证文献4

二级引证文献53

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部