In the present study, we successfully isolated PDMSCs from human placental tissues. The RT-PCR results show that PDMSCs preserved the genetic characteristics of the primitive embryonic stage--Oct-4 and Nanog. By using serum-free medium supplemented essential growth factors and induction medium culture for 4 weeks, a monolayer of spindle-like PDMSCs gradually formed 3D spheroid bodies (SB-PDMSCs). By using real-time RT-PCR, early mRNA expressions of Pdx1, as well as the Sox17 and Foxa2 genes, were observed to be significantly activated in SB-PDMSCs, followed by the expression of mature pancreas-related genes (insulin, glucagon, and somatostatin). The high insulin content of SB-PDMSCs was further confirmed by ELISA assay, and the glucose dependency was demonstrated by the corresponding insulin secretion level. In a transplantation study of streptozotocin-pretreated nude mice, the restoration of normoglycemia in the SB-PDMSC treated group was further observed. In conclusion, these results indicate that PDMSCs are an excellent source for the induced differentiation of well-functioning insulin-positive cells. The potential of these insulin producing cells derived from PDMSCs was also demonstrated functionally by the demonstration of secreted insulin in vitro and effective control of blood glucose levels in vivo.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bbrc.2007.03.157 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
BETA CELL DYSFUNCTION OCCURS INDEPENDENTLY OF INSULITIS IN TYPE 1 DIABETES PATHOGENESIS.
bioRxiv
December 2024
Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, FL, United States.
During type 1 diabetes (T1D) progression, beta cells become dysfunctional and exhibit reduced first-phase insulin release. While this period of beta cell dysfunction is well established, its cause and underlying mechanism remain unknown. To address this knowledge gap, live human pancreas tissue slices were prepared from autoantibody-negative organ donors without diabetes (ND), donors positive for one or more islet autoantibodies (AAb+), and donors with T1D within 0-4 years of diagnosis (T1D+).
View Article and Find Full Text PDFFeatures of Metabolism and Its Regulation in the Dynamics of Experimental Models of Metabolic Disorders.
Bull Exp Biol Med
December 2024
Center for Digital and Translational Biomedicine, Center for Molecular Health LLC, Moscow, Russia.
Article Synopsis
- The study examined lipid and carbohydrate metabolism as well as adipokines and growth factors in three mouse models with different metabolic disorders: alimentary obesity, leptin-resistant obesity, and diabetes mellitus.
- In the alimentary obesity model, mice showed moderate liver fat, enlarged adipose tissue, and elevated levels of glucose, adiponectin, and cholesterol.
- In the leptin-resistant model, severe tissue issues were noted, along with high blood sugar and leptin but low triglycerides and certain growth factors.
- The diabetes mellitus model revealed a decrease in insulin-producing cells and lower levels of important hormones like adiponectin and leptin, along with high insulin levels.
Investigating the pathogenicity of the recessive p.A251T variant in monogenic diabetes using iPSC-derived beta-like cells.
medRxiv
December 2024
Centre de Recherche du CHUM, and Faculty of Medicine, University of Montreal, QC, Canada.
Monogenic diabetes, formerly called Maturity-Onset Diabetes of the Young (MODY), involves single-gene mutations, typically with dominant inheritance, and has been associated with variants in 14 genes. Among these, mutations are the most common, and their diagnosis allows the use of alternative therapies, including sulfonylureas. In an earlier study, we described a variant displaying recessive transmission, p.
View Article and Find Full Text PDFA small molecule K-3 promotes PDX1 expression and potentiates the differentiation of pluripotent stem cells into insulin-producing pancreatic β cells.
Stem Cells
November 2024
School of Life Science and Technology, Institute of Science Tokyo, 4259-B-25 Nagatsuta-cho, Midori-ku, Yokohama, Kanagawa 226-8501, Japan.
Insulin-producing pancreatic β-like cells derived from human pluripotent stem cells (PSCs) are anticipated as a novel cell source for cell replacement therapy for diabetes patients. Here, we describe the identification of small molecule compounds that promote the differentiation of the PSCs into insulin-producing cells by high throughput screening with a chemical library composed of 55,000 compounds. The initial hit compound K-1 and one derivative K-3 increased the proportion of PSC-derived insulin-positive endocrine cells and their glucose-stimulated insulin secretory (GSIS) functions.
View Article and Find Full Text PDFCystic fibrosis-related diabetes is associated with reduced islet protein expression of GLP-1 receptor and perturbation of cell-specific transcriptional programs.
Sci Rep
October 2024
Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, Seattle, WA, USA.
Insulin secretion is impaired in individuals with cystic fibrosis (CF), contributing to high rates of CF-related diabetes (CFRD) and substantially increasing disease burden. To develop improved therapies for CFRD, better knowledge of pancreatic pathology in CF is needed. Glucagon like peptide-1 (GLP-1) from islet α cells potentiates insulin secretion by binding GLP-1 receptors (GLP-1Rs) on β cells.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!