MafA regulates expression of genes important to islet beta-cell function

Mol Endocrinol. 2007 Nov;21(11):2764-74. doi: 10.1210/me.2007-0028. Epub 2007 Jul 17.

Abstract

Insulin transcription factor MafA is unique in being exclusively expressed at the secondary and principal phase of insulin-expressing cell production during pancreas organogenesis and is the only transcriptional activator present exclusively in islet beta-cells. Here we show that ectopic expression of MafA is sufficient to induce a small amount of endogenous insulin expression in a variety of non-beta-cell lines. Insulin mRNA and protein expression was induced to a much higher level when MafA was provided with two other key insulin activators, pancreatic and duodenal homeobox (PDX-1) and BETA2. Potentiation by PDX-1 and BETA2 was entirely dependent upon MafA, and MafA binding to the insulin enhancer region was increased by PDX-1 and BETA2. Treatment with activin A and hepatocyte growth factor induced even larger amounts of insulin in AR42J pancreatic acinar cells, compared with other non-beta endodermal cells. The combination of PDX-1, BETA2, and MafA also induced the expression of other important regulators of islet beta-cell activity. These results support a critical role of MafA in islet beta-cell function.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Nucleus / metabolism
  • Gene Expression Regulation*
  • Glucose Transporter Type 2 / metabolism
  • HeLa Cells
  • Humans
  • Insulin / metabolism
  • Insulin-Secreting Cells / metabolism*
  • Islets of Langerhans / metabolism*
  • Maf Transcription Factors, Large / metabolism
  • Maf Transcription Factors, Large / physiology*
  • Mice
  • Models, Biological
  • Protein Binding
  • RNA, Messenger / metabolism
  • Transcriptional Activation

Substances

  • Glucose Transporter Type 2
  • Insulin
  • MAFA protein, human
  • Maf Transcription Factors, Large
  • Mafa protein, mouse
  • RNA, Messenger
  • SLC2A2 protein, human