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Surgical Research Unit, Department of Surgery, Cell Isolation and Transplantation Center, CMU, Geneva University Hospitals, 1, rue Michel-Servet, 1211 Geneva-4, Switzerland
¹ Division of Endocrinology, Diabetes and Nutrition, Geneva University Hospitals, 1211 Geneva-14, Switzerland
² Department of Genetic Medicine and Development, University Medical Center, 1211 Geneva-4, Switzerland

(Requests for offprints should be addressed to D Bosco; Email: domenico.bosco{at}medecine.unige.ch)

The aim of this study was to assess whether the expression of E-cadherin at the surface of rat ß-cells is regulated by insulin secretagogues and correlates with insulin secretion. When cultured under standard conditions, virtually all ß-cells expressed E-cadherin observed by immunofluorescence, but heterogeneous staining was observed. Using fluorescence-activated cell sorting (FACS), two ß-cell sub-populations were sorted: one that was poorly labeled (‘ECad-low’) and another that was highly labeled (‘ECad-high’). After 1-h stimulation with 16.7 mM glucose, insulin secretion (reverse hemolytic plaque assay) from individual ECad-high ß-cells was higher than that from ECad-low ß-cells. Ca²⁺-dependent ß-cell aggregation was increased at 16.7 mM glucose when compared with 2.8 mM glucose. E-cadherin at the surface of ß-cells was increased after 18 h at 11.1 and 22.2 mM glucose when compared with 2.8 mM glucose, with the greatest increase at 22.2 mM glucose + 0.5 mM isobutylmethylxanthine (IBMX). While no labeling was detected on freshly trypsinized cells, the proportion of stained cells increased in a time-dependent manner during culture for 1, 3, and 24 h. This recovery was faster when cells were incubated at 16.7 vs 2.8 mM glucose. Cycloheximide inhibited expression of E-cadherin at 2.8 mM glucose, but not at 16.7 mM, while depolymerization of actin by either cytochasin B or latrunculin B increased surface E-cadherin at low glucose. In conclusion, these results show that expression of E-cadherin at the surface of islet ß-cells is controlled by secretagogues including glucose, correlates with insulin secretion, and can serve as a surface marker of ß-cell function.