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Role of CITED2 in shaping macrophage inflammatory response

ABSTRACT: Role of CITED2 in shaping macrophage inflammatory response

PROVIDER: PRJNA622586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11467753.fastq.gz	Fastqsanger.gz
	SRR11467754.fastq.gz	Fastqsanger.gz
	SRR11467755.fastq.gz	Fastqsanger.gz
	SRR11467756.fastq.gz	Fastqsanger.gz
	SRR11467757.fastq.gz	Fastqsanger.gz

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Role of CITED2 in shaping macrophage inflammatory response

Project description:CBP/p300-interacting transactivator with glutamic acid/aspartic acid-rich carboxyl-terminal domain 2 (CITED2) is a member of the CITED family of proteins that play very critical roles in cellular development and differentiation. Several independent studies have revealed that mutation in the CITED2 gene is associated with human congenital heart defects. Concordant with these observations, experimental murine studies affirmed that mutation or loss of Cited2 resulted in congenital heart defects, as well as perturbation in the left-right patterning of the body axis. Furthermore, deficiency of Cited2 significantly impaired the development of lung, liver, placenta, and adrenal tissue at the embryonic stage (PMCID: PMC5809687).

2020-09-23 | GSE147943 | GEO

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Macrophage-CITED2 and inflammatory gene expression

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Macrophage-CITED2 and inflammatory gene expression

Project description: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.

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The role of distinct synovial tissue macrophage populations in shaping synovial tissue microenvironment

Project description:The role of distinct synovial tissue macrophage populations in shaping synovial tissue microenvironment

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Role of KLF6 in shaping macrophage inflammatory response

Project description:Kruppel-like transcription factor 6 (KLF6) is a member of zinc-finger family transcription factors that regulate critical cellular processes including development, differentiation, proliferation, and programmed cell death. Alterations in KLF6 expression or function has been associated with the pathogenesis of numerous human ailments, including inflammatory bowel diseases, cancer, hepatic steatosis, and hepatic fibrosis.

2021-01-06 | GSE136476 | GEO

Identification of CITED2 target genes in human CB

Project description:CB CD34+ cells were were transduced with control (tNGFR) or CITED2 overexpression lentivectors, or control (shSCR) or shRNA CITED2 lentivectors and mRNA was isolated in order to investigate global gene expression changes upon perturbation of CITED2. CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT3L and TPO for 12 hrs. Cells were transduced with control (tNGFR) or CITED2 overexpression lentivectors, or control (shSCR) shRNA CITED2 lentivectors, in three rounds over 48 hrs. Transduced cells were sorted after which RNA was isolated for Illumina beadhchip arrays HT12 v4.

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CITED2 restrains pro-inflammatory macrophage activation and response.

Project description:Macrophages are strategically distributed in mammalian tissues and play an essential role in priming immune response. However, macrophages need to constantly strike a balance between activation and inhibition state to avoid a futile inflammatory reaction. Herein, we identify the CBP/p300-interacting transactivator with glutamic acid/aspartic acid-rich carboxyl-terminal domain 2 (CITED2) as a potent repressor of macrophage pro-inflammatory activation. Gain- and loss-of-function studies revealed that CITED2 is required for optimal peroxisome proliferator-activated receptor gamma (PPAR?) activation and attendant select anti-inflammatory gene expression in macrophages. More importantly, deficiency of CITED2 resulted in significant attenuation in rosiglitazone-induced PPAR? activity, PPAR? recruitment to target gene promoters and anti-inflammatory target gene expression in macrophages. Interestingly, deficiency of Cited2 strikingly heightened pro-inflammatory gene expression through stabilization of hypoxia-inducible factor 1 alpha (HIF1?) protein in macrophages. Further, overexpression of Egln3 or inhibition of HIF1? in Cited2-deficient macrophages completely reversed elevated pro-inflammatory cytokine/chemokine gene expression. Importantly, mice bearing a myeloid-specific deletion of Cited2 were highly susceptible to endotoxin-induced sepsis symptomatology and mortality. Collectively, our observations identify CITED2 as a novel negative regulator of macrophage pro-inflammatory activation and protect the host from inflammatory insults.

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