Identification of CITED2 and PU.1 target genes in human CB
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE118036 | GEO | 2019/04/17
REPOSITORIES: GEO
Similar Datasets
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.
2014-09-05 | E-GEOD-47218 | biostudies-arrayexpress
Project description:CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT#L and TPO for 48 hrs. Cells were transduced with control MiNR1 or STAT5A-ER in three rounds over 48 hrs. Hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and megakaryocyte/erythroid progenitors (MEPs) were sorted (for details see Blood 2011, Fatrai et al). cells were stimulated with 100 ng/ml 4OHT for 24 hrs after which RNA was isolated for Illumina beadhchiop arrays HT12 v3
2011-01-22 | GSE26775 | GEO
Project description:CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT#L and TPO for 48 hrs. Cells were transduced with control MiNR1 or STAT5A-ER in three rounds over 48 hrs. Hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and megakaryocyte/erythroid progenitors (MEPs) were sorted (for details see Blood 2011, Fatrai et al). cells were stimulated with 100 ng/ml 4OHT for 24 hrs after which RNA was isolated for Illumina beadhchiop arrays HT12 v3 CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT#L and TPO for 48 hrs. Cells were transduced with control MiNR1 or STAT5A-ER in three rounds over 48 hrs. Hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), granulocyte/macrophage progenitors (GMPs), and megakaryocyte/erythroid progenitors (MEPs) were sorted (for details see Blood 2011, Fatrai et al). cells were stimulated with 100 ng/ml 4OHT for 24 hrs after which RNA was isolated for Illumina beadhchiop arrays HT12 v3
2011-01-22 | E-GEOD-26775 | biostudies-arrayexpress
Project description:Although it has been shown that HIF1 and 2 fulfill essential roles within the hematopoietic system and in the regulation of HSC fate, little is currently known about the specific mechanisms that are involved. We identified transcriptome changes induced by hypoxia, constitutively active HIF1(P402/564) and HIF2(P405/531) in human cord blood CD34+ cells. Thus, we were able to identify common hypoxia-HIF1-HIF2 gene signatures, but we also identified specific target genes that were exclusively regulated by HIF1, HIF2 or hypoxia. CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT3L and TPO for 48 hrs. Cells were transduced with control pRRL-IRS2-EGFP lentiviral vectors or vectors expressing HIF1α(P402A,P564A) or HIF2α(P405A,P531A) in one or two rounds of 12 hrs each. 24 hrs later transduced cells were sorted after which RNA was isolated. 5 independent CB CD34+ batches were isolated, transduced and sorted, and isolated RNA was combined and used for Illumina beadhchip arrays HT12 v4
2014-03-01 | E-GEOD-54662 | biostudies-arrayexpress
Project description:Although it has been shown that HIF1 and 2 fulfill essential roles within the hematopoietic system and in the regulation of HSC fate, little is currently known about the specific mechanisms that are involved. We identified transcriptome changes induced by hypoxia, constitutively active HIF1(P402/564) and HIF2(P405/531) in human cord blood CD34+ cells. Thus, we were able to identify common hypoxia-HIF1-HIF2 gene signatures, but we also identified specific target genes that were exclusively regulated by HIF1, HIF2 or hypoxia. CB CD34+ cells were isolated by Miltenyi miniMACS column. Cells were prestimulated in HPGM with 100 ng/ml KITL, FLT3L and TPO for 3 days after which cells were placed either at normoxia or hypoxia (1% O2 for an additional 24 hrs). 5 independent CB CD34+ batches were used and isolated RNA was combined and used for Illumina beadhchip arrays HT12 v4
2014-03-01 | E-GEOD-54661 | biostudies-arrayexpress
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.
2014-09-05 | GSE47218 | GEO
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.
2022-12-08 | GSE218217 | GEO
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
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 | GSE202337 | GEO
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 | GSE203192 | GEO