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EphA-Ephrin-A-Mediated ß cell communication regulates insulin secretion from pancreatic islets.
Cell 129, 359-370 (2007)
In vertebrates, ß cells are aggregated in the form of pancreatic islets. Within these islets, communication between ß cells inhibits basal insulin secretion and enhances glucose-stimulated insulin secretion, thus contributing to glucose homeostasis during fasting and feeding. In the search for the underlying molecular mechanism, we have discovered that ß cells communicate via ephrin-As and EphAs. We provide evidence that ephrin-A5 is required for glucose-stimulated insulin secretion. We further show that EphA-ephrin-A-mediated ß cell communication is bidirectional: EphA forward signaling inhibits insulin secretion, whereas ephrin-A reverse signaling stimulates insulin secretion. EphA forward signaling is downregulated in response to glucose, which indicates that, under basal conditions, ß cells use EphA forward signaling to suppress insulin secretion and that, under stimulatory conditions, they shift to ephrin-A reverse signaling to enhance insulin secretion. Thus, we explain how ß cell communication in pancreatic islets conversely affects basal and glucose-stimulated insulin secretion to improve glucose homeostasis.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
cellbio; humidisease
ISSN (print) / ISBN
0092-8674
e-ISSN
1097-4172
Zeitschrift
Cell
Quellenangaben
Band: 129,
Seiten: 359-370
Verlag
Cell Press
Verlagsort
Cambridge, Mass.
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Developmental Genetics (IDG)