Fig. 4
From: SWELL1 is a glucose sensor regulating β-cell excitability and systemic glycaemia
SWELL1-mediated ICl,SWELL is required for both glucose- and hypotonic swelling-induced Ca2+ signaling in MIN6 cells. a SWELL1 western blot in WT and CRISPR/Cas9-mediated Swell1 KO MIN6 cell lines (Supplementary Fig. 6b for full blots). b Current–voltage plots of SWELL1-mediated current in response to hypotonic swelling in WT and Swell1 KO MIN6 cells confirm complete ablation of hypotonic swelling-stimulated ICl,SWELL in Swell1 KO MIN6 cells. c–e Fura-2 Ca2+ transients in c WT, d Swell1 KO and e WT+nifedipine (10 µM) MIN6 cells in response to 30 mM glucose stimulation (basal 1 mM glucose). 40 mM KCl stimulation confirms cell viability and excitability. f Mean peak Fura-2 ratio in glucose-stimulated WT (n = 34), Swell1 KO (n = 36), and WT+nifedipine (n = 16) MIN6 cells. g–i Fura-2 Ca2+ transients in g WT, h Swell1 KO, and i WT+nifedipine (10 µM) MIN6 cells in response to hypotonic swelling stimulation (210 mOsm/kg; isotonic 300 mOsm/kg). j Mean peak Fura-2 ratio in swell-stimulated WT (n = 42 cells), Swell1 KO (n = 26 cells), and WT+nifedipine MIN6 cells. In the presence of VGCC blocker nifedipine (10 µM), neither glucose (e) nor hypotonic swelling (i) induced Ca2+ transients in WT MIN6 cells. Data are shown as mean ± s.e.m. One-way ANOVA for in-group comparison, unpaired t-test for between-group comparison. *p < 0.05, ***p < 0.001. ns, not significant
