MicroRNA-29a is up-regulated in beta-cells by glucose and decreases glucose-stimulated insulin secretion

被引：104

作者：

Bagge, Annika ^{[1
]}

Clausen, Trine R. ^{[2
]}

Larsen, Sylvester ^{[1
]}

Ladefoged, Mette ^{[2
]}

Rosenstierne, Maiken W. ^{[1
,4
]}

Larsen, Louise ^{[3
]}

Vang, Ole ^{[1
]}

Nielsen, Jens H. ^{[3
]}

Dalgaard, Louise T. ^{[1
]}

机构：

[1] Roskilde Univ, Dept Sci Syst & Models, DK-4000 Roskilde, Denmark

[2] Novo Nordisk, Diabet Biol, Malov, Denmark

[3] Univ Copenhagen, Dept Biomed Sci, Copenhagen, Denmark

[4] Statens Serum Inst, Dept Virol, Copenhagen, Denmark

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 426卷 / 02期

关键词：

MicroRNA; Beta-cell; Islets of Langerhans; MicroRNA-29a; Glucose toxicity; Beta-cell dysfunction; GENE-EXPRESSION; MITOCHONDRIA; ACTIVATION; CONTRIBUTE; APOPTOSIS; MIR-29A; CANCER; MODEL; MICE;

D O I：

10.1016/j.bbrc.2012.08.082

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Chronically elevated levels of glucose impair pancreatic beta-cell function while inducing beta-cell proliferation. MicroRNA-29a (miR-29a) levels are increased in several tissues in diabetic animals and mediate decreased insulin-stimulated glucose-transport of adipocytes. The aim was to investigate the impact of glucose on miR-29a levels in INS-1E beta-cells and in human islets of Langerhans and furthermore to evaluate the impact of miR-29a on beta-cell function and proliferation. Increased glucose levels up-regulated miR-29a in beta-cells and human and rat islets of Langerhans. Glucose-stimulated insulin-secretion (GSIS) of INS-1E beta-cells was decreased by forced expression of miR-29a, while depletion of endogenous miR-29a improved GSIS. Over-expression of miR-29a increased INS-1E proliferation. Thus, miR-29a up-regulation is involved in glucose-induced proliferation of beta-cells. Furthermore, as depletion of miR-29a improves beta-cell function, miR-29a is a mediator of glucose-induced beta-cell dysfunction. Glucose-induced up-regulation of miR-29a in beta-cells could be implicated in progression from impaired glucose tolerance to type 2 diabetes. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：266 / 272

页数：7

共 34 条

[31]

Roggli E., 2012, Diabetes

[32] Mitochondria and Cancer: A Growing Role in Apoptosis, Cancer Cell Metabolism and Dedifferentiation [J].

Scatena, Roberto .

ADVANCES IN MITOCHONDRIAL MEDICINE, 2012, 942 :287-308

[33]

Song Lin, 2006, Birth Defects Research, V78, P140, DOI 10.1002/bdrc.20070

[34] Identification of glucose-regulated miRNAs from pancreatic β cells reveals a role for miR-30d in insulin transcription [J].

Tang, Xiaoqing ;

Muniappan, Latha ;

Tang, Guiliang ;

Oezcan, Sabire .

RNA, 2009, 15 (02) :287-293

← 1 2 3 4 →