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Computational Reconstruction of Pancreatic Islets as a Tool for Structural and Functional Analysis
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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.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|November 6, 2007
PubMed

Insights

Epithelial (E)-cadherin (ECAD) is crucial for beta-cell communication and insulin secretion. Blocking ECAD disrupts cell signaling and significantly reduces insulin release from pancreatic islets.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Islet Physiology

Background:

  • Efficient insulin secretion from pancreatic beta-cells relies on robust intra-islet communication.
  • Epithelial (E)-cadherin (ECAD) is a cell surface adhesion protein vital for maintaining the structure of epithelial tissues, including the islets of Langerhans.

Purpose of the Study:

  • To investigate the role of ECAD in regulating insulin secretion from pancreatic pseudoislets.
  • To understand how ECAD influences intercellular communication within the islets of Langerhans.

Main Methods:

  • Utilized an insulin-secreting model system (pseudoislets).
  • Assessed the impact of immuno-neutralizing ECAD on morphology, calcium signaling (fura-2 microfluorimetry), cell-to-cell communication (Lucifer Yellow dye injection), and insulin secretion (ELISA).

Main Results:

  • Antibody blockade of ECAD diminished glucose-evoked cytosolic calcium ([Ca(2+)](i)) changes and insulin secretion.
  • ECAD neutralization disrupted the synchronicity of glucose-stimulated calcium oscillations and impaired gap junction communication, evidenced by reduced dye transfer.
  • The functional outcome of ECAD neutralization was a significant reduction in insulin secretion.

Conclusions:

  • Cell adhesion mediated by ECAD plays a distinct role in regulating intercellular communication among beta-cells within pancreatic islets.
  • Disruption of ECAD-mediated adhesion impacts beta-cell communication, with significant consequences for insulin secretion regulation.
Abstract

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