Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from thymic endothelial cells after damage

ABSTRACT: Expression data from thymic endothelial cells after damage

PROVIDER: PRJNA418719 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Expression data from thymic endothelial cells after damage (2)

Project description:Expression data from thymic endothelial cells after damage (2)

| PRJNA675085 | ENA

Expression data from thymic endothelial cells after damage

Project description:The thymus is extremely sensitive to damage but also has a remarkable ability to repair itself. However, the mechanisms underlying this endogenous regeneration remain poorly understood and this capacity diminishes considerably with age. To identify alternate regeneration pathways in the thymus, we performed an unbiased transcriptome analysis of the non-hematopoietic (CD45-) stromal cell compartment of the thymus, which is less sensitive to thymic damage compared to the CD45+ hematopoietic compartment. Recent work has suggested that ECs can contribute towards thymic regeneration via their production of so-called angiocrine factors. Using a technique to constitutively activate the Akt pathway in ECs using the pro-survival adenoviral gene E4ORF1, ECs can be propagated and expanded ex vivo (exEC) while maintaining their phenotype and vascular tube formation capacity. We compared the gene expression of freshly isolated thymic ECs and exEC-derived from the thymus.

2018-02-01 | GSE106980 | GEO

Expression data from thymic endothelial cells after damage (2)

2021-10-01 | GSE160989 | GEO

Expression data from thymic non-hematopoietic stromal cells after damage

Project description:Expression data from thymic non-hematopoietic stromal cells after damage

| PRJNA418718 | ENA

Expression data from thymic non-hematopoietic stromal cells after damage

Project description:The thymus is extremely sensitive to damage but also has a remarkable ability to repair itself. However, the mechanisms underlying this endogenous regeneration remain poorly understood and this capacity diminishes considerably with age. To identify alternate regeneration pathways in the thymus, we performed an unbiased transcriptome analysis of the non-hematopoietic (CD45-) stromal cell compartment of the thymus, which is less sensitive to thymic damage compared to the CD45+ hematopoietic compartment. Concentrating on a model of thymic damage caused by a sublethal dose of total body irradiation (SL-TBI), where after an initial depletion of thymic cellularity with regeneration initiated after a nadir between days 3-4 and complete recovery by day 42, we found significant upregulation at both days 4 and 7 of several genes known to be involved in thymic function.

2018-02-01 | GSE106981 | GEO

Next generation sequencing of thymic dendritic cells after damage

Project description:Next generation sequencing of thymic dendritic cells after damage

| PRJNA758971 | ENA

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

T cell derived LTR signal regulates thymic egress via distinct thymic portal endothelial cells

Project description:T cell derived LTR signal regulates thymic egress via distinct thymic portal endothelial cells

| PRJNA731352 | ENA

Expression data from isolated SHARPIN-deficient thymic Treg cells

Project description:Expression data from isolated SHARPIN-deficient thymic Treg cells

| PRJNA428601 | ENA

Expression data from endothelial cell

Project description:Expression data from endothelial cell

| PRJNA415176 | ENA