Extended Data Fig. 2: Accumulation of mutant CEL protein aggregates reduces proliferation and impairs function of β-cells.
From: Abnormal exocrine–endocrine cell cross-talk promotes β-cell dysfunction and loss in MODY8
a, Representative FACS plots showing percentage of AnnexinV and Zombie Near Infrared (NIR) stained β-cells treated with conditioned medium for 10 days to assess apoptosis levels (n = 3 biologically independent samples). b-d, Heatmap showing differentially expressed genes involved in cellular senescence (b), Insulin secretion (c), glycolysis/gluconeogenesis (top panel), oxidative phosphorylation (lower panel) (d) in β-cells treated with conditioned medium for 10 days (EV n = 9, WT n = 10, MUT n = 10 biologically independent samples). e, Mitochondrial respiration profile of EndoC-βH1 cells exposed to conditioned media for 10 days. Cells were challenged with oligomycin (15 μM), carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) (10 μM), and Rotenone (1.1 µM) and actinomycin (25 μM) (left panel). Quantification of basal (middle panel) and maximal respiration (right panel) capacity (EV n = 5, WT n = 4, MUT n = 5 biologically independent samples). Data are presented as mean values ± SEM. One-way ANOVA followed by Tukey’s multiple comparison (a,e).
