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Y-27632 Impairs Angiogenesis on Extra-Embryonic Vasculature in Post-Gastrulation Chick Embryos
Johannes W Duess1,2,3, Jan-Hendrik Gosemann1,2, Anna Kaskova Gheorghescu3
1Department of Pediatric Surgery, University of Leipzig, 04103 Leipzig, Germany.
Toxics
|February 28, 2023
Summary
Y-27632 treatment impairs blood vessel formation in chick embryos by inhibiting Rho-associated coiled-coil-containing protein kinase (ROCK) signaling, potentially causing ventral body wall defects due to failed angiogenesis.
Area of Science:
- Developmental Biology
- Cell Signaling
- Vascular Biology
Background:
- Rho-associated coiled-coil-containing protein kinase (ROCK) signaling regulates embryonic development, including angiogenesis, via actin cytoskeleton control.
- ROCK is crucial for vascular endothelial growth factor (VEGF) signaling pathways.
- Y-27632, a ROCK inhibitor, causes ventral body wall defects (VBWDs) in chick embryos, possibly linked to impaired angiogenesis.
Purpose of the Study:
- To investigate the effects of Y-27632 on angiogenesis in post-gastrulation chick embryos.
- To determine if Y-27632-induced angiogenesis impairment contributes to VBWDs.
Main Methods:
- Chick embryos were cultured and treated with Y-27632 or vehicle.
- Angiogenesis was assessed by observing extra-embryonic blood vessel formation and yolk sac circulation.
- Fractal analysis, Western blot, and RT-PCR were used to evaluate vascular development and molecular signaling.
Main Results:
- Y-27632 treatment led to reduced extra-embryonic blood vessel formation and impaired yolk sac circulation.
- ROCK downstream signaling was inhibited, evidenced by decreased phosphorylated myosin light chain.
- Gene expression of VEGF and VEGFR-2 increased post-treatment, with elevated VEGF protein levels observed later.
Conclusions:
- Y-27632 administration impairs angiogenesis in early chick embryos.
- Inhibition of ROCK signaling affects VEGF pathway components.
- Impaired angiogenesis is a potential mechanism contributing to Y-27632-induced VBWDs.

