Related Experiment Video
Updated: Jun 21, 2026
05:38
Isolating and Analyzing Cells of the Pancreas Mesenchyme by Flow Cytometry
Published on: January 28, 2017
One process for pancreatic beta-cell coalescence into islets involves an epithelial-mesenchymal transition
Lori Cole1, Miranda Anderson, Parker B Antin
1Department of Animal Sciences, Agricultural Research Complex, University of Arizona, 1650 East Limberlost Drive, Tucson, Arizona 85719, USA.
The Journal of Endocrinology
|July 18, 2009
Summary
Beta-cell differentiation and islet formation in diabetes mellitus treatment involve an epithelial-mesenchymal transition (EMT). This process, observed in sheep pancreas development, shows beta-cells migrating from the epithelium, acquiring mesenchymal traits.
Area of Science:
- Developmental Biology
- Endocrinology
- Cell Biology
Background:
- Islet replacement therapy for diabetes mellitus is limited by donor tissue availability.
- Expanding endocrine tissue requires understanding normal islet formation processes.
- Previous research has not fully elucidated the cellular mechanisms of beta-cell differentiation and islet formation.
Purpose of the Study:
- To compare pancreas development in sheep and humans.
- To investigate the role of epithelial-mesenchymal transition (EMT) in beta-cell differentiation and islet formation.
- To identify key transcription factors and cellular markers involved in these processes.
Main Methods:
- Comparative analysis of sheep and human pancreas development.
- Immunofluorescence staining to co-localize insulin with epithelial and mesenchymal markers.
- In situ hybridization to analyze the expression of SNAIL family genes in developing pancreatic tissue.
Main Results:
- Key transcription factors (PDX1, NGN3, NKX2-2, NKX6-1) were expressed appropriately during sheep pancreas development.
- Developing beta-cells in sheep lose epithelial markers (cytokeratin, E-cadherin, beta-catenin) and gain mesenchymal markers (vimentin).
- SNAIL1 and SNAIL2 genes were co-expressed with insulin in developing beta-cells, suggesting their role in EMT.
Conclusions:
- The study provides strong evidence for an epithelial-mesenchymal transition (EMT) in beta-cell migration from the pancreatic ductal epithelium.
- EMT is a crucial mechanism in beta-cell differentiation and the subsequent formation of pancreatic islets.
- Understanding this process may facilitate strategies for expanding endocrine tissue for diabetes therapy.
Related Concept Videos
01:05Insulin Secretory Vesicles
Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
01:27Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Insulin and C-peptide are co-secreted in...
01:23Renewal of Intestinal Stem Cells
The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...
01:28Forced Transdifferentiation
Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
Artificial transdifferentiation occurs...
Artificial transdifferentiation occurs...
01:26Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...