4.4 Article

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

期刊

RNA
卷 15, 期 2, 页码 287-293

出版社

COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1261/rna.1211209

关键词

miRNA; glucose; pancreas; MIN6; diabetes; miR-30d

资金

  1. NIDDK [K01 DK078648-01, R01DK067581]
  2. American Heart Association
  3. Great Rivers Affiliate
  4. KTRDC, USDA-NRI [2006-35301-17115, 2006-3510017433]
  5. NSF [MCB-0718029, 00000260]
  6. Kentucky Science and Technology Corporation [KSTC-144-401-08-029]
  7. National Center for Research Resources [P20RR020171]
  8. American Diabetes Association [1-05-CD-15]

向作者/读者索取更多资源

MicroRNAs (miRNAs) are small noncoding ribonucleotides that bind mRNAs and function mainly as translational repressors in mammals. MicroRNAs have been implicated to play a role in many diseases, including diabetes. Several reports indicate an important function for miRNAs in insulin production as well as insulin secretion. We have recently carried out a screen in the pancreatic beta-cell line MIN6 to identify miRNAs with altered abundance in response to changes in glucose concentrations. This screen resulted in identification of 61 glucose-regulated miRNAs from a total of 108 miRNAs detectable in MIN6 cells. Many of the identified miRNAs, including miR-124a, miR-107, and miR-30d were up-regulated in the presence of high glucose. Only a few of the miRNAs, including miR-296, miR-484, and miR-690 were significantly down-regulated by high glucose treatment. Interestingly, we found that overexpression of miR-30d, one of the miRNAs up-regulated by glucose, increased insulin gene expression, while inhibition of miR-30d abolished glucose-stimulated insulin gene transcription. Overexpression or inhibition of miR-30d did not have any effect on insulin secretion. These data suggest that the putative target genes of miR-30d may be negative regulators of insulin gene expression.

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