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Pancreatic islet transplantation has remained an effective therapy for type 1 diabetes since 2000. Its widespread use has been prohibited by the shortage of suitable donors. It is critical to explore an applicable alternative for β-cell replacement. This study was performed to generate insulin-producing cells (IPCs) from pancreas-derived mesenchymal stem cells (pMSCs). pMSCs were isolated from discarded pancreatic tissue in the filter liquor during islet isolation procedure in mice and ex vivo expanded in culture. IPCs were induced by transfection of pancreas and duodenal transcription factor 1 (PDX-1) mRNA in vitro. Some islet characteristics were identified on pMSC-derived IPCs in mRNA and protein levels. Our results demonstrated that mouse pMSCs can be transdifferentiated into effective glucose-responsive insulin-producing cells through transfecting synthetic modified PDX-1 mRNA in vitro. The study of PDX-1 mRNA-induced pMSC reprogramming may pave the way toward the development of a novel β-cell source for the treatment of diabetes.
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http://dx.doi.org/10.1007/s10238-014-0319-0 | DOI Listing |
Cell Regen
September 2025
Institute of Physical Chemistry, Polish Academy of Sciences, Warsaw, Poland.
Diabetes mellitus is a common and serious metabolic disease globally, characterized by increased blood glucose levels. The major pathogenesis is the functional impairment of insulin-producing beta cells in the pancreas and the lack of insulin secretion. Although both type 1 and type 2 diabetes develop through distinct pathological mechanisms, they lead to the destruction and/or dysfunction of beta cells, resulting in inadequate beta cell mass to maintain normal blood glucose levels.
View Article and Find Full Text PDFDiabetes Obes Metab
September 2025
Department of Integrated Traditional Chinese and Western Medicine Oncology, The Second People's Hospital of Huaihua City, Huaihua, Hunan, China.
Aims: Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing pancreatic β-cells. While T cells are well-known critical, growing evidence shows that B cells also play a key role in T1D development. T cell immunoreceptor with immunoglobulin and ITIM domain (TIGIT), as an inhibitory immune checkpoint, is important in maintaining immune homeostasis and has become a therapeutic target for several autoimmune diseases.
View Article and Find Full Text PDFBiology (Basel)
August 2025
Department of Laboratory Haematology, Metaxas Anticancer Memorial Hospital, 18537 Pireas, Greece.
Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder characterized by the destruction of insulin-producing pancreatic beta cells, resulting in lifelong insulin dependence. While genetic susceptibility-particularly human leukocyte antigen (HLA) class II alleles-is a major risk factor, accumulating evidence implicates viral infections as potential environmental triggers in disease onset and progression. This narrative review synthesizes current findings on the role of viral pathogens in T1DM pathogenesis.
View Article and Find Full Text PDFJ Mater Chem B
September 2025
Nanostructured Materials Laboratory, University of Georgia, Athens, GA, 30602, USA.
Three-dimensional cell cultures on biomimetic scaffolds have gained significant attention in tissue engineering, drug delivery, and scalable cell production. Current challenges in creating an ideal scaffold are providing maximum space for cells to grow while ensuring efficient nutrient, metabolite, and gas exchange to prevent the formation of necrotic or apoptotic regions. In our work, we grow insulin-producing INS-1 cells on touch-spun polycaprolactone (PCL) fiber scaffolds.
View Article and Find Full Text PDFJ Biol Chem
August 2025
Department of Medicine, Division of Endocrinology, Stanford University, Stanford, CA, USA; Department of Bioengineering, Stanford University, Stanford, CA, USA. Electronic address:
Pathologic loss of insulin-producing pancreatic β-cells is a hallmark of diabetes that is potentially reversible through regenerative therapy. However, existing replication-promoting compounds lack β-cell specificity, limiting their clinical application. To overcome this challenge, we generated βRepZnC, a zinc-chelating replication compound designed to leverage the uniquely high zinc content of β-cells for targeted delivery.
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