FIGURE 7

FIGURE 7

LTC4 participate in the genetic compensation for the loss of swell1 and ameliorate the hemodynamic phenotype. (A,B) Effects of cysltr1 and cysltr3 knockdown on early embryonic hemodynamics were evaluated at 30 hpf. (A) Heart rate in WT and dHetero embryos following CRISPR interference targeting cysltr1 (r1) and cysltr3 (r3). Knockdown of cysltr3 significantly reduced heart rate in WT embryos, while no significant effect was observed in dHetero embryos. (B) Vessel diameter of the dorsal aorta (DA) remained unaffected in WT embryos after cysltr1 or cysltr3 knockdown. However, cysltr1 knockdown further reduced DA diameter in dHetero embryos. (C) Rescue effects of LTC4 treatment on early hemodynamic defects at 30 hpf. Vessel diameters were unaffected in WT, but the diameter of the posterior cardinal vein was significantly increased in dHetero embryos after LTC4 treatment. The sample size (n) for each group is indicated above the scatter plot. The data were collected from two biological replicates. LTC4: vehicle control with 0.4% ethanol; +, 640 nM nifedipine. ns, no significance; *p < 0.05; **p < 0.01.