Macrophage-CITED2 and inflammatory gene expression

CITED2 is a member of the CBP/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain family of transcriptional regulators and is exclusively localized in the nucleus. Previous studies have demonstrated that CITED2 plays an important role in cellular development and differentiation. Experimental murine studies have shown that Cited2 mutation or deficiency results in congenital heart and neural crest defects, impairment in the development of lung, liver, placenta, and adrenal tissue, and perturbation in the left-right patterning of the body axis. Previous studies have also show that CITED2 is predominantly expressed in murine and human macrophages. Myeloid-specific CITED2 deficient mice are highly susceptible to lipopolysaccharide (LPS)-induced endotoxic shock syndrome, zymosan-induced lung inflammation, and experimental atherogenesis. Mechanistically, CITED2 in cooperation with PPARγ promotes anti-inflammatory gene expression while suppressing NFκB, HIF1α, STAT1, and IRF1 signaling to attenuate pro-inflammatory gene expression in macrophages. The bone marrow derived macrophges were obtained from Lyz2cre and Lyz2cre:CITED2Fl/Fl mice (n=3). Total RNA samples derived from these BMDMs were subjected to RNAseq analyses.