Search

The aim of this study was to assess whether the expression of E-cadherin at the surface of rat β-cells is regulated by insulin secretagogues and correlates with insulin secretion. When cultured under standard conditions, virtually all β-cells expressed E-cadherin observed by immunofluorescence, but heterogeneous staining was observed. Using fluorescence-activated cell sorting (FACS), two β-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 β-cells was higher than that from ECad-low β-cells. Ca2+-dependent β-cell aggregation was increased at 16.7 mM glucose when compared with 2.8 mM glucose. E-cadherin at the surface of β-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 β-cells is controlled by secretagogues including glucose, correlates with insulin secretion, and can serve as a surface marker of β-cell function.