Homotypic Cell Contact Enhances Insulin but Not Glucagon Secretion.
From: Beta Cell Development and Function Group, Division of Reproductive Health, Endocrinology and Development, Hodgkin Building, King’s College London, Guy’s Campus, London SE1 1UL, UK. helen.brereton@kcl.ac.uk
Biochemical and biophysical research communications
- Publish Date: Jun 2006
- ISSN: 0006-291X
- Volume: 344
- Issue: 3
- Pages: 995-1000
- Medium: Print
- Language: English
- Citation (JAMA): Brereton Helen C, Carvell Melanie J, Asare-Anane Henry, et al. Homotypic Cell Contact Enhances Insulin but Not Glucagon Secretion.. Biochem. Biophys. Res. Commun. Jun 2006;344:995-1000
Abstract
Intra-islet interactions influence beta-cell function, and disruption of islet architecture results in a reduction in glucose-induced insulin secretion, whereas re-aggregation improves secretory responsiveness. Our studies on MIN6 cells have shown that by configuring beta-cells as three-dimensional islet-like structures there is a marked improvement in glucose-induced insulin secretion compared to that of their monolayer equivalents. In the present study, we have used the mouse glucagon-secreting alphaTC1 cell line to see whether homotypic interactions are important in the regulation of glucagon secretion from alpha-cells. We found no significant difference in the secretory responses of alphaTC1 cells maintained as monolayers or as cell clusters. We also found that different cell adhesion molecules are involved in cell interactions between alpha- and beta-cells; MIN6 cells express ECAD, whereas alphaTC1 cells express NCAM. ECAD is necessary for cell cluster formation by MIN6 cells but not by alphaTC1 cells, whereas NCAM is not needed for the formation of cell clusters in either cell line.
Mesh Headings (Keywords): Animals, Cell Adhesion, Cell Communication, Cell Line, Glucagon, Insulin, Islets of Langerhans, Mice, Neural Cell Adhesion Molecules
Check for Full Text / PubMed Unique Identifier (PMID): 16643853
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