Figure 5. Direct activation of calcineurin promoted the optimal maturity of neonatal mouse β-cells in isolated islets in vitro.

(A–B) Glucose-induced insulin secretion from neonatal and adult mouse islets sequentially stimulated with 3 mM glucose (A) and 20 mM glucose (B) after isolation from P0 and 8-week-old mice, and for 3 days of culture in different types of media (different concentrations of glucose combined with or without CGA) in vitro. The black dotted line in A indicates the value of the ELISA kit detection limit. n = 4–10 experiments per condition. *p<0.05, **p<0.01; ns, not significant. (C) Glucose Stimulation Index (fold change in GSIS) of the mouse islets described in (A) and B). n = 4–10 experiments per condition. *p<0.05, **p<0.01; ns, not significant. (D) An illustration of the maximum amplitude of calcium influx in islets under 2.8 mM and 16.7 mM glucose stimulation. (E) Quantification of maximal amplitude of glucose-induced calcium influx in islets under different culture conditions. n = 4–7 islets per condition. *p<0.05, **p<0.01; ns, not significant. (F) Fold change in maximal amplitude of glucose-induced calcium influx in islets under stimulation and resting conditions described in (E). n = 4–7 islets per condition. *p<0.05; ns, not significant. See also Figure 5—figure supplement 1.

Figure 5—figure supplement 1. Direct activation of calcineurin promoted the optimal maturity of neonatal mouse β-cells in isolated islets in vitro, as indicated by ex vivo islet calcium imaging.

(A) The experimental design for ex vivo islet calcium imaging used in (B–C). (B–C) Representative time courses of calcium transients under indicated glucose stimulations in islets that had been cultured in media with 5.6 mM glucose (B) and 11 mM glucose (C) for 3 days with or without CGA.