PrdxI Encode Peroxiredoxin is Required for Vascular Development in Zebrafish

Abstract

Genetic signaling and redox homeostasis are required for proper growth of blood vessels. Using zebrafish as a model organism have been intensively identified many molecules that control vasculature. Some antioxidant genes have been shown important for vascular growth. However, there is still limited information about oxidative stress and vascular development during embryogenesis. Here, we report a novel function of prdx1 that play critical roles in vascular growth during zebrafish developmentPrdx1 encodes a cytosolic peroxidase responsible for the remove of hydrogen peroxide and is highly conserved from yeast to mammal. Our in situ hybridization data showed the expression pattern of prdx1 is in developing vessels. Knockdown of prdx1 by morpholino injection impairs the vascular growth of ISV (intersegmental vessel) and CVP (cardinal vein plexus). We further showed the reduction of ISV is due to a decrease of cell proliferation and migration, but not cell death. Consistent with the vascular defects in prdx1MO, we found a decreased expression of vascular markers, flt4,mrc1, stabilin and ephrinb2. Loss of prdx1 results in vascular defects suggests the antioxidant function is important. Thus, we test if oxidative stress could cause vascular defects. Our data showed H2O2 treatment impaired CVP formation and synergetic effects are showed while H2O2‐treated in prdx1MO. We also found the expression of main antioxidant genes (SOD1, SOD2, catalase and prdx2) are decreased while loss of prdx1. Finally, prdx1 likely regulates hemangioblast fate decision because the increased expression of blood marker gata1 concurrent with the decreased expression of endothelial markers in prdx1 MO. Together, we showed a novel function of prdx1 that play critical roles in vascular growth during zebrafish development.