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Cholangiocytic cysts (CCs) treated with or without vasoactive intestinal peptide (VIP)

ABSTRACT: Cholangiocytic cysts (CCs) treated with or without vasoactive intestinal peptide (VIP)

PROVIDER: PRJNA580026 | ENA |

REPOSITORIES: ENA

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Cholangiocytic cysts (CCs) treated with or without vasoactive intestinal peptide (VIP)

Project description:Transcriptional profiling of CCs derived from embryonic day (E) 13.5 wild type (WT) mouse hepatoblasts treated with or without VIP.

2020-01-05 | GSE139519 | GEO

Transcriptional effects of VIP on murine intestinal stem cells

Project description:In our study, we investigated the effect of Vasoactive intestinal peptide (VIP) on murine intestinal stem cell (ISC) activity and differentiation in homeostatic conditions and following irradiation-induced injury. We utilized a model of murine intestinal organoids and observed that VIP promotes epithelial differentiation towards a secretory phenotype predominantly via the p38 MAPK pathway. Moreover, VIP prominently modulates epithelial proliferation as well as the number and proliferative activity of Lgr5-EGFP+ ISC under homeostatic conditions. Further analysis revealed that in vitro acute irradiation injury renders Lgr5-EGFP+ ISC even more susceptible to modulations by VIP, which results in the strong promotion of epithelial regeneration by VIP. Finally, these effects by VIP translate into an in vivo model of abdominal irradiation, where VIP was shown to prominently mitigate radiation-induced injury. Taken together, our findings indicate a prominent role of VIP in modulating ISC behavior in intestinal homeostasis and its potential to promote intestinal regeneration following acute irradiation injury.

2024-09-27 | GSE261001 | GEO

Identification of the Early VIP Transriptome and its Associated Interactome in Activated Murine CD4 T Cells

Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Activated Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the presence of PMA/ionomycin (activated) for five hours with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. PMA/ionomycin (activated) mouse CD4 T spleenocytes with VIP ligand (sample) vs. PMA/ionomycin (activated) mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.

2010-01-09 | E-GEOD-18525 | biostudies-arrayexpress

Identification of the Early VIP Transriptome and its Associated Interactome in Resting Murine CD4 T Cells

Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Resting Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the absence of PMA/ionomycin (resting) with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. Naïve mouse CD4 T spleenocytes with VIP ligand (sample) vs. naïve mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.

2010-01-09 | E-GEOD-18524 | biostudies-arrayexpress

Identification of the Early VIP Transriptome and its Associated Interactome in Resting Murine CD4 T Cells

2010-01-09 | GSE18524 | GEO

Identification of the Early VIP Transriptome and its Associated Interactome in Activated Murine CD4 T Cells

2010-01-09 | GSE18525 | GEO

DUSP4 regulates input to the suprachiasmatic circadian network via VIP-induced activation of the ERK1/2 pathway

Project description:Analysis of the genes and cellular signalling cascades mediating the response of SCN slices to vasoactive intestinal peptide (VIP). Primary goal was to find novel genes that may be involved in circadian phase shifting for further study. Promoter analysis of significantly regulated genes and gene ontology analysis would provide information into pathways VIP acts through in the SCN.

2019-02-07 | GSE113797 | GEO

A novel hippocampal long-range VIP-GABAergic projection to subiculum contributes to fear memory formation through region-specific connectivity

Project description:We sequenced seven long-range projection vasoactive intestinal peptide (VIP)-expressing interneurons from the mouse CA1 oriens/alveus area using patch-seq technique to determine their molecular identity.

2018-01-30 | GSE109755 | GEO

PKHD1-deficient human induced pluripotent stem (iPS) cell-derived cholangiocyte-like cells (PKHD1-KO CCs) vs heterozygously mutated PKHD1 human iPS cell-derived cholangiocyte-like cells (PKHD1-Hetero CCs)

Project description:Transcriptional profiling of PKHD1-KO and PKHD1-Hetero CCs. PKHD1-deficient (PKHD1-KO) and heterozygously mutated PKHD1 iPS clones were established by RNA-guided genome editing using CRISPR/Cas9 system. The iPS clones were differentiated into cholangiocyte-like cells in cysts (cholangiocytic cysts, CCs) in a 3D-culture system.

2019-03-19 | GSE125871 | GEO

Rathke’s Cleft-Like Cysts Arise From Isl1 Deletion in Murine Pituitary Progenitors

Project description:The transcription factor ISL1 is expressed in pituitary gland stem cells and the thyrotrope and gonadotrope lineages. Pituitary-specific Isl1 deletion causes hypopituitarism with increased stem cell apoptosis, reduced differentiation of thyrotropes and gonadotropes, and reduced body size. Conditional Isl1 deletion causes development of multiple Rathke’s cleft-like cysts, with 100% penetrance. Foxa1 and Foxj1 are abnormally expressed in the pituitary gland and associated with a ciliogenic gene expression program in the cysts. We confirmed expression of FOXA1, FOXJ1 and stem cell markers in human Rathke's cleft cyst tissue, but not craniopharyngiomas, which suggests these transcription factors are useful, pathological markers for diagnosis of Rathke's cleft cysts. These studies support a model whereby expression of ISL1 in pituitary progenitors drives differentiation into thyrotropes and gonadotropes, and without it, activation of FOXA1 and FOXJ1 permits development of an oral epithelial cell fate with mucinous cysts. This pituitary-specific Isl1 mouse knockout sheds light on the etiology of Rathke's cleft cysts and the role of ISL1 in normal pituitary development.

2020-04-22 | GSE149019 | GEO

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