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Vasculogenic defects of great vessels (GVs) are a major cause of congenital cardiovascular diseases. However, genetic regulators of endothelial precursors in GV vasculogenesis remain largely unknown. Here we show that Stat4, a transcription factor known for its regulatory role of pro-inflammatory signalling, promotes GV vasculogenesis in zebrafish. We find  stat4  transcripts highly enriched in  nkx2.5   +   endothelial precursors in the pharynx and demonstrate that genetic ablation of  stat4  causes stenosis of pharyngeal arch arteries (PAAs) by suppressing PAAs 3–6 angioblast development. We further show that  stat4  is a downstream target of  nkx2.5  and that it autonomously promotes proliferation of endothelial precursors of the mesoderm. Mechanistically,  stat4  regulates the emerging PAA angioblasts by inhibiting the expression of  hdac3  and counteracting the effect of  stat1a . Altogether, our study establishes a role for Stat4 in zebrafish great vessel development, and suggests that Stat4 may serve as a therapeutic target for GV defects.

The pro-inflammatory signalling regulator Stat4 promotes vasculogenesis of great vessels derived from endothelial precursors