P-selectin axis plays a key role in microglia immunophenotype and glioblastoma progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA658598 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12493241.fastq.gz | Fastqsanger.gz | |||
| SRR12493242.fastq.gz | Fastqsanger.gz | |||
| SRR12493243.fastq.gz | Fastqsanger.gz | |||
| SRR12493244.fastq.gz | Fastqsanger.gz | |||
| SRR12493245.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 48 |
Similar Datasets
Project description:We aimed to evaluated the effect of P-Selectin knockdown in glioblastoma cells on their tumorigenesis and the brain microenvironment. To that end, we have established P-Selectin knockdown GL261 glioblastoma cells by shRNA. For control, scrambled shRNA was used (NC). P-Selectin kncockdown and NC GL261 cells were inoculated intra-cranially into mice. 16-21 days post tumor cell inoculation, cancer cells and cells of the tumor microenvironment were isolated using magnetic beads cell separation. We showed meaningful changes in gene expression and cluster distributions between the groups.
2021-02-22 | GSE156663 | GEO
Project description:Glioblastoma (GB) is a highly invasive type of brain cancer exhibiting poor prognosis. As such, its microenvironment plays a crucial role in its progression. Among the brain stromal cells, the microglia were shown to facilitate GB invasion and immunosuppression. However, the reciprocal mechanisms by which GB cells alter microglia/macrophages behavior are not fully understood. We propose that these mechanisms involve adhesion molecules such as the Selectins family. These proteins are involved in immune modulation and cancer immunity. We show that P-selectin mediates microglia-enhanced GB proliferation and invasion by altering microglia/macrophages activation state. We demonstrate these findings by pharmacological and molecular inhibition of P-selectin which leads to reduced tumor growth and increased survival in GB mouse models. Our work sheds light on tumor-associated microglia/macrophage function and the mechanisms by which GB cells suppress the immune system and invade the brain, paving the way to exploit P-selectin as a target for GB therapy.
| S-EPMC7997963 | biostudies-literature
Project description:We used microarrays to detail the global gene expression in peritoneal macrophages (PM) from E-selectin+/+ and E-selectin-/- mouse infected with Listeria Monocytogenes in vivo on day3
2018-01-25 | GSE90808 | GEO
Project description:During aging, hematopoietic stem cell (HSC) function progressively declines which can lead to reduced blood cell production and regeneration, impaired lymphoid cell production and ineffective erythropoiesis. In this study, we uncovered that during aging the cell surface presentation of the type-1 transmembrane protein P-selectin (CD62P, encoded by Selp) increases in a large fraction of HSCs. Notably, expression of P-selectin molecularly and functionally dichotomized the aging HSC pool; stem cells presenting with high abundance of P-selectin were hallmarked by aging-associated gene expression programs and reduced repopulation upon regenerative stress. Overexpression of Selp in young HSCs was sufficient to impair long-term reconstitution potential and repress erythropoiesis. Moreover, IL-1β, which is chronically elevated in the aged bone marrow, triggered Selp expression in HSCs. The aged transcriptome, including Selp, was largely restored when aged HSCs were transplanted to young mice. Mechanistically, we uncovered that appropriate stimulation of P-selectin by its primary ligand, P-selectin glycoprotein ligand-1 (PSGL-1), suppressed aging-associated gene expression and reversely, lack of P-selectin signaling led to HSC premature aging. Collectively, our study uncovered a novel functional role of P-selectin engagement in regulating HSC regeneration and driving stem cell aging when perturbed.
2025-03-21 | GSE269360 | GEO
Project description:Single-cell dissection of the genotype-immunophenotype relationship in glioblastoma
| PRJNA1145992 | ENA
Project description:LK immunophenotype cells after sleep deprivation.
| PRJNA1176548 | ENA
Project description:Tumor cell extravasation takes place, similar to leukocytes, in a multi-step process by which cells emigrate from the blood stream through the vascular endothelium into the tissue. Selectins are regarded as the most important molecules for the first capturing step of the cascade. Whether all tumor cells employ selectin dependent adhesion to metastasize or there is an alternative mechanism still is an open question. Comparative transcriptomic analysis of OVCAR8 and SKOV3 cultured cells and revealed that one third of genes encoding proteins involved in the selectin dependent leukocyte like adhesion cascade show lower expression levels in OVCAR8 cultured cells in comparison to that in SKOV3 cultured cells. In contrast to SKOV3 cells, c-Fos overexpression in OVCAR8 cells does not significantly influence expression of the leukocyte like adhesion cascade genes leaving them at similar levels as in control OVCAR8 cells. The intraperitoneal xenograft model of OVCAR8 cells demonstrated that aggressiveness of OVCAR8-derived tumors is not dependent of c-Fos expression level and comparable with that for SKOV3 control tumors. Based on transcriptome array data we analyzed in details expression of genes encoding proteins involved in the leukocyte like adhesion cascade, E- and P-selectin ligands, as well as glycosylation enzymes in both type of tumors. Our results suggest that selectin-dependent mechanism is not the only for adhesion of OVCAR8 ovarian cancer cells. There is at least one additional mechanism of extravasation that does not rely on selectins.
2017-03-31 | GSE97226 | GEO
Project description:Pediatric Sickle Cell Disease Humoral Immunophenotype Alterations
| PRJNA1092746 | ENA
Project description:For patients with chronic limb-threatening ischemia and limited revascularization options, alternate means for therapeutic angiogenesis and limb salvage are needed. E-selectin is a cell adhesion molecule that is critical for inflammation and neovascularization in areas of wound healing and ischemia. Here, we tested the efficacy of modifying ischemic limb tissue by intramuscular administration of E-selectin/AAV2/2 (adeno-associated virus serotype 2/2) to modulate angiogenic and inflammatory responses in a murine hindlimb gangrene model. Limb appearance, reperfusion, and functional recovery were assessed for 3 weeks after induction of ischemia. Mice receiving E-selectin/AAV2/2 gene therapy had reduced gangrene severity, increased limb and footpad perfusion, enhanced recruitment of endothelial progenitor cells, and improved performance on treadmill testing compared to control group. Histologically, E-selectin/AAV2/2 gene therapy was associated with increased vascularity and preserved myofiber integrity. E-selectin/AAV2/2 gene therapy also upregulated a panel of pro-angiogenic genes yet downregulated another group of genes associated with the inflammatory response. This novel gene therapy did not induce adverse effects on coagulability, or hematologic, hepatic, and renal function. Our findings highlight the potential of E-selectin/AAV2/2 gene therapy for improving limb perfusion and function in patients with chronic limb-threatening ischemia.
2022-04-29 | GSE201479 | GEO
Project description:For patients with chronic limb-threatening ischemia and limited revascularization options, alternate means for therapeutic angiogenesis and limb salvage are needed. E-selectin is a cell adhesion molecule that is critical for inflammation and neovascularization in areas of wound healing and ischemia. Here, we tested the efficacy of modifying ischemic limb tissue by intramuscular administration of E-selectin/AAV2/2 (adeno-associated virus serotype 2/2) to modulate angiogenic and inflammatory responses in a murine hindlimb gangrene model. Limb appearance, reperfusion, and functional recovery were assessed for 3 weeks after induction of ischemia. Mice receiving E-selectin/AAV2/2 gene therapy had reduced gangrene severity, increased limb and footpad perfusion, enhanced recruitment of endothelial progenitor cells, and improved performance on treadmill testing compared to control group. Histologically, E-selectin/AAV2/2 gene therapy was associated with increased vascularity and preserved myofiber integrity. E-selectin/AAV2/2 gene therapy also upregulated a panel of pro-angiogenic genes yet downregulated another group of genes associated with the inflammatory response. This novel gene therapy did not induce adverse effects on coagulability, or hematologic, hepatic, and renal function. Our findings highlight the potential of E-selectin/AAV2/2 gene therapy for improving limb perfusion and function in patients with chronic limb-threatening ischemia.
2022-04-29 | GSE201476 | GEO