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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).

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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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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 is a conserved regulator of deep placentation (Human)

Project description:Establishment of the hemochorial placentation site requires the exodus of trophoblast cells from the placenta and their transformative actions on the uterine vasculature, which is a critical but poorly understood developmental process. CBP/p300-interacting transactivator with glutamic acid/aspartic acid-rich carboxyl terminal domain 2 (CITED2) is a member of the CITED protein family of co-regulators and has been shown to possess roles in embryogenesis, including placenta development. We examined the involvement of CITED2 in the rat, which exhibits deep hemochorial placentation, a feature it shares with the human. CITED2 is distinctively expressed in the junctional zone compartment of the rat placentation site and in intrauterine invasive trophoblast cells. Homozygous disruption of the rat Cited2 locus resulted in placental and fetal growth restriction and abnormalities in heart and lung development, which are also characteristic of the CITED deficient mouse model. However, other features of the mouse Cited2 null phenotype, including exencephaly, adrenal gland agenesis, and prenatal lethality were not associated with CITED2 deficiency in the rat. Trophoblast-specific lentiviral CITED2 knockdown in the rat yielded a growth arrested placental phenotype. Smaller Cited2 null placentas were associated with a growth restricted junctional zone and coincided with a delay in intrauterine trophoblast cell invasion. Invasive trophoblast cells arise from the junctional zone. Transcriptomes of the junctional zone, the invasive trophoblast cell lineage, and differentiating trophoblast stem cells were affected by CITED2 disruption, as were placental adaptations to hypoxia and exposure to viral mimetics. Evidence for the conservation of CITED2 expression in human placental tissue and conserved actions in invasive/extravillous trophoblast cell development were demonstrated. We conclude that CITED2 is a conserved regulator of deep hemochorial placentation.

2023-05-18 | GSE202336 | GEO

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