NID1 mitigates the effects of hypoxia on pancreatic β‐cells and increases insulin secretion. A,B) Expression pattern of BM proteins, insulin (INS), and DAPI in human (A) fetal (11 weeks postgestation) and (B) adult pancreas (64 years). Scale bars: 20 µm. Highly magnified images show the colocalization of NID1 with INS in native adult pancreas. Scale bar: 5 µm. C) Quantification of the colocalization of ECM proteins with INS (n = 10), one‐way ANOVA with Tukey's multiple comparisons test. D) GSIS response (with 0 × 10−3 and 20 × 10−3
m glucose) under normoxic conditions of human NID1‐treated pseudoislets in suspension at different concentrations: 20, 30, 40 µg mL−1 when compared with the control (PBS) (n = 5); two‐way ANOVA with Tukey's multiple comparisons test. E) E‐cadherin expression under normoxic conditions (n ≥ 5). F) Cell death under normoxic conditions via the detection of cleaved caspase‐3 (n = 14) and TUNEL+ cells (n = 7). G) GSIS response (with 0 × 10−3 and 20 × 10−3
m glucose) under hypoxic conditions of NID1‐treated pseudoislets at 30 µg mL−1 and normalized by live cells (n = 10); two‐way ANOVA with Tukey's multiple comparisons test. H) E‐cadherin expression under hypoxic conditions (n ≥ 5 m; unpaired t‐test. I) Protective effect of NID1 assessed by cleaved caspase‐3 expression (n ≥ 7). and via detection of TUNEL+ cells (n ≥ 4); unpaired t‐test. *p < 0.05; **p < 0.01, ***p < 0.001, and ****p < 0.0001.