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E-GEOD-62741

ABSTRACT: Thymic T-cell progenitor development is supported by membrane bound Kit ligand provided by a combined vascular endothelial and epithelial niche.

OTHER RELATED OMICS DATASETS IN: PRJNA265043

PROVIDER: E-GEOD-62741 | ExpressionAtlas | 2019-05-14

REPOSITORIES: ExpressionAtlas

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Bi-directional signaling by membrane-bound KitL induces proliferation and co-ordinates thymic endothelial cell and thymocyte expansion

Project description:The ligand for the c-Kit receptor, KitL, exists as a membrane-associated (mKitL) and a soluble form (sKitL). KitL functions outside c-Kit activation have not been identified. We show that co-culture of c-Kit– and mKitL–expressing NIH3T3 cells results in signaling through mKitL: c-Kit–bound mKitL recruits calcium-modulating cyclophilin ligand (CAML) to selectively activate Akt, leading to CREB phosphorylation, mTOR pathway activation, and increased cell proliferation. Activation of mKitL in thymic vascular endothelial cells (VECs) induces mKitL- and Akt-dependent proliferation, and genetic ablation of mKitL in thymic VECs blocks their c-Kit responsiveness and proliferation during neonatal thymic expansion. Therefore, mKitL–c-Kit form a bi-directional signaling complex that acts in the developing thymus to coordinate thymic VEC and early thymic progenitor (ETP) expansion by simultaneously promoting ETP survival and VEC proliferation. This mechanism may be relevant to both normal tissues and malignant tumors that depend on KitL–c-Kit signaling for their proliferation.

2018-11-21 | PXD011061 | Pride

Mus musculus

Project description:Thymic T-cell progenitor development is supported by membrane bound Kit ligand provided by a combined vascular endothelial and epithelial niche.

| PRJNA265043 | ENA

Thymic T-cell progenitor development is supported by membrane bound Kit ligand provided by a combined vascular endothelial and epithelial niche.

Project description:Gene expression analysis of purified KitL-tomato+ and KitL-tomato- thymic vascular endothelial cells, cortical and medullary thymic epithelial cells from 5 weeks old male kitL-tomato reporter mice Differentially expressed genes analysis of thymic stromal cells

2016-01-18 | E-GEOD-62741 | biostudies-arrayexpress

Thymic T-cell progenitor development is supported by membrane bound Kit ligand provided by a combined vascular endothelial and epithelial niche.

2016-01-18 | GSE62741 | GEO

RNA-seq on cells with or without pathogenic PAX1 variants at different stages of in vitro differentiation into thymic epithelial progenitor cells

Project description:Bi-allelic, loss-of-function PAX1 variants underlie a syndromic form of severe combined immunodeficiency (SCID) by disrupting thymus development. To assess if bi-allelic PAX1 variants affect differentiation of thymic epithelial cells in vitro, we reprogrammed fibroblasts from a healthy control and two patients with bi-allelic pathogenic PAX1 variants to induced pluripotent stem cells (iPSCs), and subsequently differentiated these to thymic epithelial progenitor cells (TEP).

2020-02-15 | GSE138784 | GEO

Female mice lacking Pald1 exhibit endothelial cell apoptosis and emphysema

Project description:Paladin (Pald1, mKIAA1274 or x99384) was identified in screens for vascular-specific genes and is a putative phosphatase. We have demonstrated that paladin has a predominant vascular expression pattern and shifts from endothelial to mural cells during mouse development. We have now characterized the Pald1 knock-out mouse in a broad array of behavioral, physiological and biochemical tests. Here, we show that female, but not male, Pald1 heterozygous and homozygous knock-out mice displayed an emphysema-like phenotype with increased alveolar air spaces and impaired lung function with obstructive changes. In contrast to many other tissues where Pald1 is restricted to the vascular compartment, Pald1 is expressed in both the epithelial and mesenchymal compartments of the postnatal lung. However, in Pald1 knock-out females, there is a specific increase in apoptosis and proliferation of endothelial cells, but not in non-endothelial cells. This results in a transient reduction of endothelial cells in the maturing lung. Our data suggests that paladin is required during lung vascular development and for normal function of the developing and adult lung in a sex-specific manner. To our knowledge, this is the first report of a sex-specific effect on endothelial cell apoptosis. Proteomic analysis of Pald1 wild type and knock-out mice reveal that most of the protein expression differences are related to sex and not genotype, supporting the notion that sex can be a major factor for lung development and disease. In addition, Pald1 wild type and knock-out mice exhibit differential expression of HPGD, hydroxyprostaglandin dehydrogenase 15 (NAD), the major enzyme for degradation of prostaglandins.

2017-11-01 | PXD005625 | JPOST Repository

mRNA-seq of mouse lung vascular endothelial cells and mouse liver sinusoidal endothelial cells before and after their partial reprogramming into progenitor-like cells and recellularization of decellularized mouse lung scaffolds

Project description:In this study we developed highly proliferative and lineage restricted lung endothelial derived progenitor-like cells using the transient expression of Yamanaka factors via doxycycline inducible system combined with LIF-supplemented media. We investigate the potential of these induced progenitor-like cells for the vascular engineering of the lungs. Our results show that these cells recapitulate the segment specific heterogeneity in the decellularized lung scaffolds and show immediate recovery of endothelial genes after recellularization.

2020-06-23 | E-MTAB-8394 | biostudies-arrayexpress

Developmental dynamics of two bipotent progenitors of thymic epithelium

Project description:T cell development in the thymus is essential for cellular immunity and depends on the organotypic thymic epithelial microenvironment. Compared to other organs, the size and cellular composition of the thymus is unusually dynamic, exemplified by rapid growth and high T cell output during early stages of development, followed by a gradual loss of functional thymic epithelial cells and diminished naïve T cell production with age. Single-cell RNA sequencing (scRNA-seq) has uncovered an unexpected heterogeneity of cell types in the thymic epithelium of young and aged adult mice; however, the identities and developmental dynamics of putative pre- and postnatal epithelial progenitors have remained unresolved. Here, we combine scRNA-seq and a novel CRISPR/Cas9-based cellular barcoding system in mice to determine qualitative and quantitative changes in the thymic epithelium over time. This dual approach enabled us to identify two principal progenitor populations: an early bi-potent progenitor type biased towards cortical epithelium, and a postnatal bi-potent progenitor population biased towards medullary epithelium. We further demonstrate that continuous autocrine provision of Fgf7 leads to sustained expansion of thymic microenvironments without exhausting the epithelial progenitor pools, suggesting a strategy to modulate the extent of thymopoietic activity.

2022-03-30 | GSE106856 | GEO

RNA-seq analysis on thymic stromal cells

Project description:We performed RNA sequencing (RNA-seq) on thymic fibroblasts, thymic epithelial cells, endothelial cells, pericytes, dendritic cells, and lymph node fibroblastic reticular cells.

2020-03-24 | GSE147357 | GEO

LTβR controls thymic portal endothelial cells for hematopoietic progenitor cell homing and T cell regeneration

Project description:Continuous thymic homing of hematopoietic progenitor cells (HPCs) via the blood is critical for normal T cell development. However, the nature and the differentiation program of the specialized thymic endothelial cells (ECs) controlling this process remain poorly understood. Here, using conditional gene-deficient mice, we find that lymphotoxin beta receptor (LTβR) directly controls thymic ECs to guide HPC homing. Interestingly, T cell deficiency or conditional ablation of T-cell-engaged LTβR signaling results in a defect in thymic HPC homing, suggesting the feedback regulation of thymic progenitor homing by thymic products. Furthermore, we identify and characterize a special thymic portal EC population with features that guide HPC homing. LTβR is essential for the differentiation and homeostasis of these thymic portal ECs. Finally, we show that LTβR is required for T cell regeneration upon irradiation-induced thymic injury. Together, these results uncover a cellular and molecular pathway that governs thymic EC differentiation for HPC homing.

2017-02-09 | GSE83114 | GEO

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