Fig 2: BMPER ameliorates brain injury and decreases cell death after MCAO. (A)The Kaplan‐Meier survival curve of MCAO mice receiving different doses of recombinant BMPER (5, 50 and 100 μg/kg). *p<0.05, **p < 0.01 by log‐rank test. NS, no significance. (B) TTC staining showed the brain infarct area of MCAO mice receiving recombinant BMPER (50 μg/kg). (C) Body weight of MCAO mice receiving recombinant BMPER. Data in B&C are expressed as mean ± SEM, n = 8, *p < 0.05, **p < 0.01 by Student's t‐test. (D) Brain water content in mice receiving recombinant BMPER (50 μg/kg). Data are expressed as mean ± SEM, n = 8. **p < 0.01 by ANOVA followed by LSD‐t post hoc test. (E) Neurological deficit evaluation in mice receiving recombinant BMPER (50 μg/kg) using Bederson scoring and Garcia scoring. Data are expressed as mean ± SEM, n = 8. *p < 0.05, **p < 0.01 by Kruskal–Wallis test. (F) TUNEL assay showing the cell death in penumbra area of MCAO mice receiving BMPER treatment. Data are expressed as mean ± SEM, n = 11. **p < 0.01 by ANOVA followed by LSD‐t post hoc test. Scale bar = 100 μm. (G–I) The activities of caspase‐3, caspase‐8, and caspase‐9 in penumbra area of MCAO mice treated by recombinant BMPER. Data are expressed as mean ± SEM, n = 8. **p < 0.01 by ANOVA followed by LSD‐t post hoc test. BMP, bone morphogenetic protein; BMPER, BMP‐binding endothelial regulator; DAPI, 4′,6‐diamidino‐2‐phenylindole; MCAO, middle cerebral artery occlusion; NS, no significance; TUNEL, terminal deoxynucleotidyl transferase dUTP nick‐end labeling