Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq of renal CD64+CD11b+F4/80hi from adult mice after cisplatin-induced acute kidney injury

ABSTRACT: We use bulk RNA sequencing of sorted cells to characterize the gene expression profiles of renal MHCII+/-D11b+F4/80hi cells 72 hours after cisplatin-induced acute kidney injury (AKI). F4/80hi cells are activated after cisplatin induced AKI and start to downregulate MHCII on transcriptional level. Downregulation of MHCII is probably caused by a downregulation/inhibition of its most important transcriptional activator Ciita

ORGANISM(S): Mus musculus

PROVIDER: GSE135921 | GEO | 2020/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNAseq of renal CD64+CD11b+F4/80hi from adult mice after cisplatin-induced acute kidney injury

Project description:RNAseq of renal CD64+CD11b+F4/80hi from adult mice after cisplatin-induced acute kidney injury

| PRJNA560645 | ENA

RNAseq of renal dendritic cells from adult Clec9a-Cre Rosa-YFP mice

Project description:We use bulk RNA sequencing of sorted cells to characterize the gene expression profiles of renal dendritic cell (DC) subsets, cDC1 and cDC2, as well as MHCII+CD64+ F4/80hi and MHCII+CD64+ CD11bhi cells. Splenic DCs and red pulp macrophages serve as reference populations for a macrophage-like or DC-like phenotype. By sorting YFP+/YFP- F4/80hi or YFP+/YFP- CD11bhi cells from Clec9a-Cre Rosa-YFP mice we aim to reveal transcriptional differences between YFP-labelled and unlabelled cells. We showed that F4/80hi cells resemble macrophages on a transcriptional level, despite their DC origin, and that renal CD11bhi cells are a transcriptionally unique subset. However, we were not able to reveal differences between YFP+ and YFP- populations.

2020-01-31 | GSE131751 | GEO

CD102- MHCII+ (F4/80lo) resident peritoneal macrophages exhibit limited sexual dimporphism in gene expression

Project description:CD102- MHCII+ (F4/80lo) peritoneal macrophages were FACS-sorted from unmanipulated male and female C57BL/6 mice and compared by RNAseq.

2022-04-14 | GSE200630 | GEO

Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

Project description:Background – Acute kidney injury (AKI) is a devastating clinical condition affecting at least two-thirds of critically ill patients and among these patients is associated with a greater than 60% risk of mortality. Kidney mononuclear phagocytes (MP) are necessary for pathogenesis and healing in mouse models of AKI and thus have been the subject of investigation as potential targets for clinical interventions. Methods and Results – We have determined that, after injury, F4/80Hi-expressing kidney resident macrophages (KRM) are a distinct cellular subpopulation that does not differentiate from non-resident infiltrating MP. However, if KRM are depleted using polyinosinic:polycytidylic acid (poly I:C), they can be reconstituted from bone marrow derived precursors. Further, KRM lack major histocompatibility complex class II (MHCII) expression before post-parturition day 7 (P7) but upregulate it over the next 14 days. This MHCII- KRM phenotype reappears after injury. RNA sequencing shows injury causes transcriptional reprogramming of KRM to more closely resemble that found at P7. Post-injury KRM are also enriched in Wingless-type MMTV integration site family (Wnt) signaling, indicating a pathway vital for mouse and human kidney development is active. Conclusions – These data indicate that mechanisms involved in kidney development may be active after injury in KRM.

2019-04-16 | GSE121410 | GEO

Critical Role of Synovial Tissue-resident Macrophage Niche in Joint Homeostasis and Suppression of Chronic Inflammation

Project description:During synovial tissue homeostasis, both monocyte-derived F4/80int, and self-renewing F4/80hi tissue-resident, macrophage populations were identified. In contrast, in HUPO mice, decreased synovial tissue-resident macrophages preceded chronic arthritis, opened a niche permitting the influx of activated monocytes, which differentiated into F4/80hi macrophages.

2021-01-13 | GSE158446 | GEO

Murine macrophages: Peritoneal exudate macrophages (PECs) vs tumor-associated macrophages (TAMs)

Project description:Transcriptional landscape of two different TAMs subsets (F4/80hi and F4/80lo) FACS-sorted from fibrosarcoma-bearing WT mice in comparison with control macrophages (PEC)

2021-04-01 | GSE167413 | GEO

Xanthomonas sp. F4 strain:F4

Project description:Xanthomonas sp. F4 strain:F4 Genome sequencing

| PRJNA546667 | ENA

Halorubrum sp. F4 strain:F4

Project description:Halorubrum sp. F4 strain:F4 Genome sequencing and assembly

| PRJNA893763 | ENA

Nonomuraea sp. F4 strain:F4

Project description:Nonomuraea sp. F4 strain:F4 Genome sequencing and assembly

| PRJNA278762 | ENA

Proteomic analysis of cisplatin exposure on the kidney cortex proteome and the effect of preconditioning

Project description:Acute kidney injury and nephrotoxicity are important clinical side effects of cisplatin. Thus, the mechanisms of this disease, and potential treatment options are important to understand in their entity. Here, we analyzed the proteome of cisplatin induced acute kidney injury in a mouse model. Functionally we found that calorie restriction was able to completely blunt Cisplatin induced AKI, and hypoxia ameliorated cCisplatin induced AKI. To investigate the mechanism for this in high throughput, we performed label-free single-shot proteomic analyses of these kidneys.Acute kidney injury and nephrotoxicity are important clinical side effects of cisplatin. Thus, the mechanisms of this disease, and potential treatment options are important to understand in their entity. Here, we analyzed the proteome of cisplatin induced acute kidney injury in a mouse model. Functionally we found that calorie restriction was able to completely blunt Cisplatin induced AKI, and hypoxia ameliorated cCisplatin induced AKI. To investigate the mechanism for this in high throughput, we performed label-free single-shot proteomic analyses of these kidneys.

2020-01-30 | PXD005525 | Pride

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