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Updated: Jan 3, 2026

Computational Reconstruction of Pancreatic Islets as a Tool for Structural and Functional Analysis
Published on: March 9, 2022
E-cadherin and cell adhesion: a role in architecture and function in the pancreatic islet
Gareth J Rogers1, Matthew N Hodgkin, Paul E Squires
1Molecular Physiology Group, Biomedical Research Institute, Department of Biological Sciences, University of Warwick Coventry, UK.
Background/Aims:
The efficient secretion of insulin from beta-cells requires extensive intra-islet communication. The cell surface adhesion protein epithelial (E)-cadherin (ECAD) establishes and maintains epithelial tissues such as the islets of Langerhans. In this study, the role of ECAD in regulating insulin secretion from pseudoislets was investigated.
Methods:
The effect of an immuno-neutralising ECAD on gross morphology, cytosolic calcium signalling, direct cell-to-cell communication and insulin secretion was assessed by fura-2 microfluorimetry, Lucifer Yellow dye injection and insulin ELISA in an insulin-secreting model system.
Results:
Antibody blockade of ECAD reduces glucose-evoked changes in [Ca(2+)](i) and insulin secretion. Neutralisation of ECAD causes a breakdown in the glucose-stimulated synchronicity of calcium oscillations between discrete regions within the pseudoislet, and the transfer of dye from an individual cell within a cell cluster is attenuated in the absence of ECAD ligation, demonstrating that gap junction communication is disrupted. The functional consequence of neutralising ECAD is a significant reduction in insulin secretion.
Conclusion:
Cell adhesion via ECAD has distinct roles in the regulation of intercellular communication between beta-cells within islets, with potential repercussions for insulin secretion.
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