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Bulk RNA sequencing and analysis of sorted murine lung endothelial cells from WT, DNMAML, and Notch1f/f mice

ABSTRACT: We assessed the transcriptional profiles of sorted lung endothelial cells from WT, DNMAML, and Notch1f/f mouse models. The goal of the study is to determine the signaling pathways downstream of Notch signaling that are involved in the regulation of pulmonary vascular permeability

ORGANISM(S): Mus musculus

PROVIDER: GSE245264 | GEO | 2024/09/30

REPOSITORIES: GEO

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Bulk RNA sequencing and analysis of sorted Common Lymphoid Progenitor (CLP) cells from WT, Notch1+/-, and Notch1+/ΔTAD adult mouse bone marrow

Project description:We assessed the transcriptional profiles of sorted CLP cells from the bone marrow of WT and Notch hypomorphic genetic mouse models. The goals of the study are determine the signaling pathways downstream of Notch signaling in bone marrow CLPs to determine pathways involved in Notch dependent priming towards the T cell lineage.

2024-11-22 | GSE189370 | GEO

Bulk RNA sequencing and analysis of sorted fetal liver hematopoietic stem cells from VavCre+Jag1 f/f and WT E14.5 C57bl/6 embryos

Project description:We assesed the transcriptional profiles of sorted SLAM-LSK hematopoietic stem cells (HSCs) during expansion in the murine fetal liver from WT and Jag1-null mutants at embryonic day 14.5 post-conception. The goals of the study are to compare the expression profiles of rapidly proliferating fetal HSCs when the Notch ligand Jag1 is specifically deleted in the hematopoietic compartment. We find that hematopoietic deletion of Jag1 negatively impacts the expression of critical hematopoietic cell fate and identity genes such as GATA2, Mllt3 and Hoxa7. Our study establishes a unique role for Notch signaling activation in the fetal liver by the hematopoietic Jag1 ligand.

2023-07-25 | GSE186190 | GEO

Endothelial cell senescence exacerbates pulmonary hypertension by inducing juxtacrine Notch signaling in smooth muscle cells

Project description:Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a progressive increase in pulmonary artery pressure caused by pathological pulmonary artery remodeling. Here, we show that endothelial cell (EC) senescence plays a negative role in pulmonary hypertension via juxtacrine interaction with smooth muscle cells (SMCs). By using EC-specific progeroid mice that we recently generated, we discovered that EC progeria deteriorated vascular remodeling in the lungs, and exacerbated pulmonary hypertension in mice exposed to chronic hypoxia. Mechanistically, senescent ECs overexpressed Notch ligands, which resulted in increased Notch signaling and activated proliferation and migration capacities in neighboring SMCs. Pharmacological inhibition of Notch signaling reduced the effects of senescent ECs on SMCs functions in vitro, and improved the worsened pulmonary hypertension in EC-specific progeroid mice in vivo. Our findings show that EC senescence is a critical disease-modifying factor in PAH and that EC-mediated Notch signaling is a pharmacotherapeutic target for the treatment of PAH, particularly in the elderly.

2023-04-30 | GSE228491 | GEO

Time course RNA-seq profiling in sorted endothelial, epithelial, and immune cells from WT C57BL6 mice

Project description:The respiratory system undergoes remarkable structural, biochemical, and functional changes necessary for adaptation to air breathing at birth. To identify dynamic changes in gene expression in the diverse pulmonary cells at birth, we performed Drop-seq based massive parallel single-cell RNA sequencing. An iterative cell type identification strategy was used to unbiasedly identify the heterogeneity of murine pulmonary cell types on postnatal day 1. Distinct populations of epithelial, endothelial, and immune cells were identified, each containing distinct subpopulations. Cell type predictions and signature genes identified using Drop-seq were cross-validated using an independent single cell isolation platform. Temporal changes in RNA expression patterns were compared before and after birth to identify signaling pathways selectively activated in specific pulmonary cell types, demonstrating activation of UPR signaling during perinatal adaptation of the lung. Present data provide the first single cell view of the adaptation to air breathing after birth. All data from the present study are freely accessed at https://www.lungmap.net/

2019-03-29 | GSE128985 | GEO

Expression data from LSK WT, GMP WT and GMP NcstnKO

Project description:Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2 To determine other role of Notch signaling in HSC we designed a conditional mouse model of Nicastrin deletion. WT and KO HSC were analysed to determined genes controlled by Notch signaling. Bone marrow lineage negative, cKit+, Sca1+ and lineage negative, cKit+, Sca1- CD34+ FcgammaRII/III+ cells were sorted from WT and Ncstn KO littermates for RNA extraction and hybridization on Affymetrix microarrays

2011-05-12 | E-GEOD-27811 | biostudies-arrayexpress

Reduced Notch signaling in BBB vascular endothelial cells mediates high fat diet-induced alterations in brain glucose uptake and insulin signaling

Project description:Short term transition to high-fat diet (HFD) feeding causes rapid changes in the molecular architecture of the blood-brain-barrier (BBB), BBB permeability and brain glucose uptake. However, the precise mechanisms responsible for these changes remain elusive. Here we detected a rapid downregulation of Notch signaling after short-term HFD feeding. Conversely, Notch activation restores HFD-fed mouse serum induced reduction of Glut1 expression and glycolysis in cultured brain microvascular endothelial cells (BMECs). Selective, inducible expression of Notch-intracellular domain (IC) in BMECs prevents HFD-induced reduction of Glut1 expression and hypothalamic glucose uptake. Caveolin (Cav)-1 expression in BMECs is increased upon short term HFD feeding. However, NotchICBMECs mice display reduced caveola formation and BBB permeability. This ultimately translates into reduced hypothalamic insulin transport, action and systemic insulin sensitivity. Collectively, we highlight a critical role of Notch-signaling in the pleiotropic effects of short-term dietary transitions on BBB functionality.

2025-04-01 | GSE210620 | GEO

Expression data from LSK WT and LSK N1-C+

Project description:Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2 To determine other role of Notch signaling in HSC we designed a conditional mouse model of Notch activation. WT and N1-IC+ HSC were analysed to determined genes controlled by Notch signaling. Bone marrow lineage negative, cKit+, Sca1+ cells were sorted from WT and N1-IC+ littermates for RNA extraction and hybridization on Affymetrix microarrays

2011-05-12 | E-GEOD-27799 | biostudies-arrayexpress

Expression data from LSK WT and LSK NcstnKO

Project description:Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2 To determine other role of Notch signaling in HSC we designed a conditional mouse model of Nicastrin deletion. WT and KO HSC were analysed to determined genes controlled by Notch signaling. Bone marrow lineage negative, cKit+, Sca1+ cells were sorted from WT and Ncstn KO littermates for RNA extraction and hybridization on Affymetrix microarrays

2011-05-12 | E-GEOD-27794 | biostudies-arrayexpress

Bulk population RNA-sequencing of sorted stromal cell populations from murine mammary tumours

Project description:Bulk cell population transcriptomic profiling of sorted stromal cell populations from mouse mammary PyMT adenocarcinomas

2021-11-02 | GSE160561 | GEO

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis [bulk RNA-Seq]

Project description:Endothelial TGFβ signaling is one of the primary drivers of atherosclerosis-associated vascular inflammation. Inhibition of endothelial TGFβ signaling in hyperlipidemic mice reduces vessel wall inflammation and vascular permeability and leads to arrest of disease progression and regression of established lesions. We performed scRNAseq method to examine endothelial cell gene expression profile using Apoe and EC specific TGFbR1/2 KO in Apoe background mice.

2019-08-26 | GSE134555 | GEO

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