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Experimental Diabetes Research
Volume 2012 (2012), Article ID 672013, 10 pages
http://dx.doi.org/10.1155/2012/672013
Research Article

Combined Transfection of the Three Transcriptional Factors, PDX-1, NeuroD1, and MafA, Causes Differentiation of Bone Marrow Mesenchymal Stem Cells into Insulin-Producing Cells

1Department of General Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China
2Department of Surgical Comprehensive Laboratory, Affiliated Hospital of Nantong University, Nantong 226001, China

Received 24 December 2011; Revised 1 April 2012; Accepted 30 April 2012

Academic Editor: Joseph R. Landolph Jr.

Copyright © 2012 Guo Qing-Song et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Aims. The goal of cell transcription for treatment of diabetes is to generate surrogate β-cells from an appropriate cell line. However, the induced replacement cells have showed less physiological function in producing insulin compared with normal β-cells. Methods. Here, we report a procedure for induction of insulin-producing cells (IPCs) from bone marrow murine mesenchymal stem cells (BM-mMSCs). These BM-mMSCs have the potential to differentiate into insulin-producing cells when a combination of PDX-1 (pancreatic and duodenal homeobox-1), NeuroD1 (neurogenic differentiation-1), and MafA (V-maf musculoaponeurotic fibrosarcoma oncogene homolog A) genes are transfected into them and expressed in these cells. Results. Insulin biosynthesis and secretion were induced in mMSCs into which these three genes have been transfected and expressed. The amount of induced insulin in the mMSCs which have been transfected with the three genes together is significantly higher than in those mMSCs that were only transfected with one or two of these three genes. Transplantation of the transfected cells into mice with streptozotocin-induced diabetes results in insulin expression and the reversal of the glucose challenge. Conclusions. These findings suggest major implications for cell replacement strategies in generation of surrogate β-cells for the treatment of diabetes.