Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression of human littoral cells and splenic vascular endothelial cells from the spleens of normal individuals and patients with myelofibrosis

ABSTRACT: The vascular lining cells in the human spleens include littoral cells (LCs) and other splenic vascular endothelial cells (SVECs). LCs that comprise about 30 percent of the splenic red pulp are specialzed endothelial cells distinct from SVECs. They line the splenic sinusoids and function as the filters and scavengers for senescent or altered red blood cells. Patients with advanced forms of myelofibrosis (MF) often develope extramedullary hematopoiesis in the spleen.Vascular lining cells within MF spleens are thought to serve as a supportive microenvironment for MF hematopoietic cells. In this study we isolated MF and normal LCs and SVECs from human spleens using immunostaining and flow cytometric sorting and used microarrays to analyze the underling mechanism of LCs' unique functions that distinguish them from SVECs, and the properties of MF LCs and SVECs and their contributions to the microenvironment of MF spleens.

ORGANISM(S): Homo sapiens

PROVIDER: GSE106532 | GEO | 2018/05/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression of human splenic littoral cells compared with splenic vascular endothelial cells

Project description:Splenic littoral cells (SLCs) are specialized endothelial cells (ECs) lining the sinusoids of the human spleen and function as the filters and scavengers for senescent or altered red blood cells. In this study we isolated SLCs and vascular ECs from normal human spleens using immunostaining and flow cytometric sorting. We used microarrays to analyze the underling mechanism of SLC’s unique functions that distinguish themm from splenic vascular ECs and identified sets of differentially expressed genes

2017-12-08 | GSE92368 | GEO

Aging-triggered iron-rich insoluble protein aggregates in the spleen originate chiefly from red pulp macrophages.

Project description:Both iron homeostasis and erythropoiesis are known to be affected by aging. Iron needs in mammals are met primarily by iron recycling from senescent red blood cells (RBCs), a task chiefly accomplished by red pulp macrophages (RPMs) in the spleen. Given that RPMs continuously process iron, their cellular functions might be susceptible to age-dependent decline, a possibility that has been unexplored to date. In our project, we identified a formation of undegradable iron- and heme-rich extracellular aggregates in the spleens of 10-11-month-old female mice. To better understand the origin of these aggregates, here, we performed: i) protein identification and intrasample quantification (iBAQ) of proteins of magnetically-isolated red pulp macrophages from spleens of two female 8-weeks-old C57BL/6J (maintained on a standard diet) and ii) label-free quantification of proteins of the splenic protein aggregates formed in the mouse spleen 24 hours after intraperitoneal iron dextran injection, using dextran-injected mice as a control. Two 8-week-old C57BL/6J mice per group were analyzed. This dataset is related to the project PXD032900, which describes quanytitative analysis of proteins in aggregates magnetically isolated from spleen of aged (standard or iron-reduced diet) and young mice (standard diet).

2023-02-02 | PXD038660 | Pride

Gene expression profiles of primary LN3 T-ALL cells and wild-type T-lineage cells from the thymus and spleen

Project description:T cell acute lymphoblastic leukemia (T-ALL) develops spontaneously in the thymus of LN3 mice and infiltrates secondary organs, including spleen. We found leukemia-associated myeloid cells from the spleens of overtly sick LN3 mice significantly support survival of splenic T-ALL cells, but not tumor-free splenic CD8+ T cells, in vitro. To determine gene signatures induced in T-ALL cells by tumor-supportive myeloid cells, but not induced in wild-type T cells, we transcriptionally profiled primary LN3 T-ALL cells from leukemic mice and T-lineage cells from tumor-free mice, isolated from thymuses and spleens, via RNA-sequencing.

2020-07-22 | GSE150096 | GEO

Homo sapiens

Project description:Gene expression profiles from human splenic macrophages, sinusoid lining cells and HUVECs

| PRJNA284415 | ENA

Identification of COX-2 as a major actor of transcriptomic adaptation of endothelial and tumor cells to cyclic hypoxia

Project description:Tumor hypoxia is not a stable phenomenon but cycles between periods of deep hypoxia and reoxygenation. Cyclic hypoxia originates from heterogeneities in red blood cell flux and from the permanent remodelling of the angiogenic vascular network. Endothelial cells lining tumor blood vessels are therefore also influenced by cyclic hypoxia. The gene expression pattern promoted by cyclic hypoxia differs from those observed under normoxia and even continuous hypoxia. PTGS2 is one gene exquisitely up-regulated in endothelial cells (and tumor cells) in response to cyclic hypoxia. Elevated COX-2 (the PTGS2 gene product) expression and activity account for cyclic hypoxia-driven increase in endothelial cell survival and angiogenesis.

2009-12-24 | GSE12246 | GEO

Eumyc and WT NK cells

Project description:Eumyc lymphoma was inoculated i.v. into C57BL/6J mice. Spleens were harvested from healthy or Emyc lymphoma-bearing mice at day 14 post-inoculation, and splenic NK cells were purfied using flow cytometry.

2020-09-01 | GSE121448 | GEO

Homo sapiens

Project description:Gene expression of human splenic littoral cells compared with splenic vascular endothelial cells

| PRJNA357361 | ENA

Gene expression of human littoral cells and splenic vascular endothelial cells from the spleens of normal individuals and patients with myelofibrosis

Project description:Gene expression of human littoral cells and splenic vascular endothelial cells from the spleens of normal individuals and patients with myelofibrosis

| PRJNA417120 | ENA

Decellularized splenic matrix as a scaffold for spleen bioengineering

Project description:The spleen is considered a non-essential organ. However, its importance is increasingly clear, given the serious disorders caused by its absence or dysfunction, e.g., greater susceptibility to infections, thromboembolism and cancer. Also, non-functionality of the spleen can lead to higher risk of infection and death in patients with serious diseases, such as HIV, myeloma, and leukemia. Surgical techniques to preserve the spleen and maintain splenic function have become increasingly common. However, the morbidity and mortality associated with its absence and dysfunction are still high. We used the decellularization technique to obtain a viable splenic scaffold for recellularization in vitro and propose the idea of bioengineered spleen transplantation to the host. In our study, we demonstrated that the scaffold created after decellularization presents good removal of residual DNA and SDS, which are essential to prevent immunogenic responses and transplantation failure. Also, the main components of the splenic matrix, such as collagens, glycoproteins, and proteoglycans, were preserved. We observed the maintenance of important structural components such as white pulp, marginal zone and red pulp, in addition to the network of vascular ducts. The scaffold we developed was subsequently recellularized with stromal cells from the spleen of neonatal rats, demonstrating adhesion, proliferation and viability of cells in contact with the scaffold. Therefore, the splenic scaffold is very promising for use in studies on spleen reconstruction and transplantation, with the aim of complete recovery of splenic function.

2021-07-15 | PXD020363 | JPOST Repository

Splenic bridging channel dendritic cells survey red blood cells for missing self-CD47

Project description:In vivo exposure of mouse CD4+ splenic DCs to sheep red blood cells causes prompt induction of multiple genes associated with DC activation.

2015-10-01 | GSE71165 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data