Differentiation of rat pancreatic duct stem cells into insulin-secreting islet-like cell clusters through BMP7 inducement.

To cure the epidemic of diabetes, in vitro produced β-like cells are lauded for cell therapy of diabetic patients. In this regard, we investigated the effects of different concentrations of bone morphogenetic protein 7 (BMP7) on the differentiation of rat pancreatic ductal epithelial-like stem cells (PDESCs) into β-like cells. For inducement of the differentiation, PDESCs were cultured in the basal media (H-DMEM + 10 % FBS + 1% penicillin-streptomycin) supplemented with 5 ng/mL, 10 ng/mL, 15 ng/mL, and 20 ng/mL of BMP7 for 28 days.

Different combinations of GABA, BMP7, and Activin A induced the in vitro differentiation of rat pancreatic ductal stem cells into insulin-secreting islet-like cell clusters.

Aims: We investigated the in vitro differentiation of adult rat PDESCs into β-like cells through supplementation of different combinations of GABA, BMP7, and Activin A in basic culture media.

Materials And Methods: The PDESCs were cultured using different inducement combinations for 28 days and microscopy, dithizone (DTZ) staining, immunohistochemical staining, real-time PCR, and glucose-stimulated insulin secretion (GSIS) assay were used to delineate the differentiation inducement potential of these combinations.

Key Findings: The results show that after 28 days, the PDESCs were differentiated into ICCs containing insulin-secreting β-like cells in different groups treated with A + B, A + G, B + G, and A + B + G but not in the control group.

Therapeutic Potentials of MicroRNAs for Curing Diabetes Through Pancreatic β-Cell Regeneration or Replacement.

MicroRNAs are a type of noncoding RNAs that regulates the expression of target genes at posttranscriptional level. MicroRNAs play essential roles in regulating the expression of different genes involved in pancreatic development, β-cell mass maintenance, and β-cell function. Alteration in the level of miRNAs involved in β-cell function leads to the diabetes.

Gimmicks of gamma-aminobutyric acid (GABA) in pancreatic β-cell regeneration through transdifferentiation of pancreatic α- to β-cells.

In vivo regeneration of lost or dysfunctional islet β cells can fulfill the promise of improved therapy for diabetic patients. To achieve this, many mitogenic factors have been attempted, including gamma-aminobutyric acid (GABA). GABA remarkably affects pancreatic islet cells' (α cells and β cells) function through paracrine and/or autocrine binding to its membrane receptors on these cells.

Pancreatic β-cell replacement: advances in protocols used for differentiation of pancreatic progenitors to β-like cells.

Insulin-producing cells derived from in vitro differentiation of stem cells and non-stem cells by using different factors can spare the need for genetic manipulation and provide a cure for diabetes. In this context, pancreatic progenitors differentiating to β-like cells garner increasing attention as β-cell replacement source. This kind of cell therapy has the potential to cure diabetes, but is still on its way of being clinically useful.