Fig. 3.

Neratinib blocks MST1 activation and apoptosis in human islets. Human islets were exposed to diabetogenic conditions (a, c, d IL-1β/IFNγ, b–d mixture of 22.2 mM glucose and 0.5 mM palmitate (HG/Palm)) ± neratinib for 72 h. a, b Phospho-MST1 (pMST1; pThr183), caspase-3 cleavage, and GAPDH or actin were analyzed by western blotting. Representative Western blots of four different human islet donors (a, b; upper panels) and pooled quantitative densitometry analysis (a, b; lower panels) of six different human islet donors are shown (n = 6). c, d β-cell apoptosis analyzed by triple staining of TUNEL (black nuclei), insulin (green), and dapi (blue). Scale bar, 100 μm. An average number of 40,420 insulin-positive β-cell per condition was counted in 3–4 independent experiments from 3 to 4 different human islet donors (n = 3–4). Results shown are means ± SEM. *p < 0.05 IL/IF or HG/Pal to control, **p < 0.05 neratinib to vehicle-treated islets under the same diabetogenic conditions; all by Student’s t tests. Source data are provided as a Source Data file