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The mammalian Mediator complex consists of over 30 subunits and functions as a transcriptional hub integrating signaling for tissue-specific gene expression. Although the role of the Mediator complex in transcription has been extensively investigated, the functions of distinct Mediator subunits in development are not well understood. Here, we dissected the role of the Mediator subunit Med23 in mouse cardiovascular development. Endothelial-specific  Med23  deletion caused embryonic lethality before embryonic day 13.5 (E13.5). The mutant embryos exhibited intracranial hemorrhage and diminished angiogenesis with dilated blood vessels in the head region, where the expression of Med23 was abundant at E10.5.  Med23  deficiency impaired vasculogenesis in the head region and impeded retinal angiogenesis. Knocking down  Med23  in human umbilical vein endothelial cells (HUVECs) resulted in angiogenic defects, recapitulating the vascular defects in  Med23 -mutant mice in a cell-autonomous manner. RNA sequencing in HUVECs indicated that  Med23  deficiency resulted in the interruption of angiogenesis and the upregulation of angiopoietin2 (Ang2), an inducing factor for vascular network instability. Inhibition of Ang2 partially rescued angiogenic sprouting and lumen dilation defects in tube formation assays. Collectively, our findings demonstrate that Med23 promotes angiogenesis and maintains vascular integrity, in part by suppressing Ang2 signaling.

Med23 supports angiogenesis and maintains vascular integrity through negative regulation of angiopoietin2 expression