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Konstantinova, I.* ; Nikolova, G.* ; Ohara-Imaizumi, M.* ; Meda, P.* ; Kucera, T.* ; Zarbalis, K. ; Wurst, W. ; Nagamatsu, S.* ; Lammert, E.*

EphA-Ephrin-A-Mediated ß cell communication regulates insulin secretion from pancreatic islets.

Cell 129, 359-370 (2007)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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
Sprache englisch
Veröffentlichungsjahr 2007
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0092-8674
e-ISSN 1097-4172
Zeitschrift Cell
Quellenangaben Band: 129, Heft: , Seiten: 359-370 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Developmental Genetics (IDG)
POF Topic(s) 30204 - Cell Programming and Repair
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-500500-001
PubMed ID 17448994
DOI 10.1016/j.cell.2007.02.044
Erfassungsdatum 2007-04-20
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