Fig. 8.

Fig. 8.

FK506 rescues the cerebral hemorrhage and CtA angiogenic defects in dyrk1aa^krb1 mutants. (A) The cerebral hemorrhage of dyrk1aa^krb1 mutant embryos (arrows) was rescued by the treatment of 50 ng/ml FK506. (B) The cerebral hemorrhage in dyrk1aa^krb1 mutant embryos at 52 hpf (40.5%) was reduced to 17.8% and 13.4% by the treatment of 50 ng/ml and 100 ng/ml FK506, respectively. No differences were seen in WT with the same treatments. (C) The compiled confocal microscopy images of CtAs in the Tg(kdrl:EGFP) background showed that CtA defects in dyrk1aa^krb1 embryos were rescued by FK506 treatment in a dose-dependent manner, and CtA angiogenesis in WT was also affected. (D) The reduced mean percentage of CtA length of dyrk1aa^krb1 mutants (75.5%) was significantly rescued up to 84.6% by 50 ng/ml FK506, whereas that of mutant branching points (74.3%) was significantly rescued up to 96.4% by 100 ng/ml FK506 at 52 hpf, compared to WT embryos as 100%. 50 ng/ml FK506 treatment increased the WT CtA length up to 110.3%, whereas 100 ng/ml FK506 treatment increased both length and branching points of WT CtAs (109.5% and 133.8%, respectively). *P<0.05, **P<0.01, ***P<0.005 (one-way ANOVA). n.s., not significant. Data are mean±s.e.m. Scale bars: 100 µm in A; 50 µm in C.