PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation.

Despite the global impact of macrophage activation in vascular disease, the underlying mechanisms remain obscure. Here we show, with global proteomic analysis of macrophage cell lines treated with either IFNγ or IL-4, that and regulate macrophage activation. In primary macrophages, Pduanyu379 and Pduanyu3714 have opposing roles in macrophage activation. Pduanyu3714 silencing induces pro-inflammatory genes and phosphorylation in M(IFNγ) cells, whereas it suppresses anti-inflammatory gene expression and phosphorylation in M(IL-4) cells. Pduanyu379 silencing suppresses pro-inflammatory genes and duanyu18131 phosphorylation in M(IFNγ) cells. Pduanyu3714 induces ADP-ribosylation of which is suppressed by Mutations at these ADP-ribosylation sites lead to increased phosphorylation. Network analysis links with human coronary artery disease. Pduanyu3714 deficiency in haematopoietic cells accelerates the development and inflammatory burden of acute and chronic arterial lesions in mice. These findings suggest that Pduanyu379 and Pduanyu3714 cross-regulate macrophage activation.

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