Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mapping of bone marrow sample proteome of Pinch1/2 knockout mice

ABSTRACT: Mesenchymal stromal cells (MSCs) are used to treat infectious and immune diseases and disorders; however, its mechanism(s) remain incompletely defined. Here we find that MSCs lacking Pinch1/2 proteins display dramatically reduced ability to suppress lipopolysaccharide (LPS)-induced acute lung injury and dextran sulfate sodium (DSS)-induced inflammatory bowel disease in mice. Mice with Pinch loss in MSCs have severe defects in both immune and hematopoietic functions, resulting in premature death, which can be restored by intravenous injection of wild-type but not Pinch-deficient MSCs.

INSTRUMENT(S): timsTOF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Stem Cell, Bone Marrow

DISEASE(S): Bacterial Sepsis

SUBMITTER: Tailin He

LAB HEAD: Tailin He

PROVIDER: PXD043019 | Pride | 2023-12-08

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ZE295LQ.rar	Other
	ZE295LQ_Con_GS.raw	Raw
	ZE295LQ_Con_SQ.raw	Raw
	ZE295LQ_KO_GS.raw	Raw
	ZE295LQ_KO_SQ.raw	Raw

Items per page:

1 - 5 of 6

Similar Datasets

Murine BM neutrophil WT vs KI experiment 1

Project description:Murine neutrophils derived from bone marrow of wild-type and cPLA2alpha-knockin mice (with the C1P interaction site of cPLA2alpha ablated) proteomes were compared

2023-10-24 | PXD039415 | Pride

Proteomic analysis of bone-marrow derived macrophages from NPC1 KO mice

Project description:Niemann-Pick type C (NPC) disease is an inherited lysosomal storage disorder mainly driven by mutations in NPC1 gene, causing lipid accumulation within late endosomes/lysosomes, and resulting in progressive neurodegeneration. To study the effect of NPC1 deficiency on the innate immune system, we performed proteomics on bone-marrow derived macrophages (BMDMs) of NPC1 KO and WT mice. Without further treatment or activation, BMDMs of NPC1 KO mice showed alterations mainly related to cholesterol metabolism, which is in line with the intracellular cholesterol transport function of NPC1.

2024-12-05 | PXD056249 | Pride

Mouse WT vs. A20 KO BMDM differential proteomics

Project description:A20 is a negative regulator of NF-κB signaling, crucial to control inflammatory responses and ensure tissue homeostasis. A20 is thought to restrict NF-κB activation both by its ubiquitin-editing activity as by non-enzymatic activities. Besides its role in NF-κB signaling, A20 also acts as a protective factor inhibiting apoptosis and necroptosis. Because of the ability of A20 to both ubiquitinate and deubiquitinate substrates and its involvement in many cellular processes, we hypothesized that deletion of A20 might generally impact on protein levels, thereby disrupting cellular processes. We performed a differential proteomics study of bone marrow derived macrophages (BMDMs) from control and myeloid-specific A20 knockout mice, both in untreated conditions and after LPS and TNF treatment, and demonstrate proteome-wide changes in protein expression upon A20 deletion. Several inflammatory proteins are up-regulated in the absence of A20, even without an inflammatory stimulus. Depending on the treatment and the time, more proteins are regulated. Together these changes may affect multiple signaling pathways disturbing tissue homeostasis and inducing (autoimmune) inflammation, as suggested by genetic studies in patients.

2018-05-15 | PXD008726 | Pride

Expression data of mouse hematopoietic cells, Nr4a1/3 wild type and double mutant

Project description:We investigate the cellular and molecular mechanisms of tumor suppression by NR4A1 and NR4A3, and show a cell intrinsic essential function in maintenance of hematopoietic stem cell (HSC) homeostasis. In the absence of Nr4a1/3, HSC lost quiescence, became highly proliferative leukemia-stem cell (LSC) that transplanted AML to recipient mice. We further revealed that loss of NR4A1/3 leads to deregulated expression of the key cell cycle regulator Cdkn1c (P57), c-Myc oncogene, and glucose metabolic genes leading to enhanced aerobic glycolysis or Warburg effect in LSCs. Reintroduction of Nr4a1 in LSCs restored HSC quiescence, and reversed Nr4a1/3 deficiency induced P57 suppression and c-Myc overexpression. Collectively, we identify an essential role of Nr4a1/3 in coordinately regulating cell cycle entry and glucose metabolism to prevent uncontrolled stem cell proliferation and AML transformation. These results have major implications for designing therapeutic strategies in AML. To identify NR4A-dependent molecular signaling pathways that may control HSC homeostasis, we performed genome-wide transcript profiling of Lin-Sca1+ (LS) cells from WT and DKO mice. For Affymetrix analysis, we generated three independent pools of RNA from sorted LS cells from 10-20 WT or DKO (2- to 3-week-old) mice per sample.

2013-12-30 | E-GEOD-31042 | biostudies-arrayexpress

The Secretome of Liver X Receptor Agonist Treated Early Outgrowth Cells Decreases Atherosclerosis in Ldlr-/- Mice

Project description:Endothelial progenitor cells (EPCs) promote the maintenance of the endothelium by secreting vasoreparative factors. A population of EPCs known as early outgrowth cells (EOCs) are being investigated as novel cell-based therapies for the treatment of cardiovascular disease. We previously demonstrated that the absence of liver x receptors (LXRs) is detrimental to the formation and function of EOCs under hypercholesterolemic conditions. Here, we investigate whether LXR activation in EOCs is beneficial for the treatment of atherosclerosis. EOCs were differentiated from the bone marrow of wildtype (WT) and LXR-knockout (Lxrαβ-/-) mice in the presence of vehicle or LXR agonist (GW3965). This data set is a proteomic comparison of EPCs at day 1 after isolation and day 9 of GW39565 treatment compared to day 9 of vehicle treatment.

2021-09-09 | PXD021993 | Pride

Quantitative proteomics reveals tissue-specific, infection-induced and species-specific neutrophil protein signatures – Candida albicans infection experiment

Project description:Neutrophils are one of the first responders to infection and are a key component of the innate immune system through their ability to phagocytose and kill invading pathogens, secrete antimicrobial molecules and produce extracellular traps. Neutrophils are produced in the bone marrow, circulate within the blood and upon immune challenge migrate to the site of infection. We wanted to understand whether this transition shapes the mouse neutrophil protein landscape, how the mouse neutrophil proteome is impacted by systemic infection and perform a comparative analysis of human and mouse neutrophils. Using quantitative mass spectrometry we reveal tissue-specific, infection-induced and species-specific neutrophil protein signatures. We show a high degree of proteomic conservation between mouse bone marrow, blood and peritoneal neutrophils, but also identify key differences in the molecules that these cells express for sensing and responding to their environment. Systemic infection triggers a change in the bone marrow neutrophil population with considerable impact on the core machinery for protein synthesis and DNA replication along with environmental sensors. We also reveal profound differences in mouse and human blood neutrophils, particularly their granule contents and their receptor repertoires. Our proteomics data provides a valuable resource for understanding neutrophil function and phenotypes across species and model systems.

2024-03-13 | PXD044556 | Pride

Deep proteome analysis of mouse brains from wild-type, LPS-induced, and drug-treated mice groups

Project description:We studied the effect of bacterial Lipopolysaccharides on inducing neuroinflammation in mice. In addition, we investigated the effect of novel LAT1-utilizing anti-inflammatory derivatives on reversing this LPS-induced neuroinflammation status. Thus, we performed deep proteome analysis of mouse brains after treatment with vehicle, LPS, and LPS with LAT1-utilizing derivatives. The objective is to follow the different inflammatory biomarkers in the mouse brain and explain the inflammatory process after the LPS treatment with and without the LAT1-utilizing prodrugs.

2022-10-25 | PXD030838 | Pride

Neddylation is a global orchestrator of the molecular network driving Schwann cell myelination

Project description:Axonal myelination is essential for neuronal function and health. In peripheral nerves, deficient myelination is responsible for the morbidity of various forms of inherited or acquired neuropathies, including Charcot-Marie-Tooth disease and diabetic neuropathy. Decades of research have uncovered a complex transcriptional and post-transcriptional program that co-ordinates the formation and maintenance of the myelin sheath. In contrast, much less is known about the functional role of post-translational modification (PTM) of proteins in this remarkable biogenic process. Neddylation, a PTM that involves the conjugation of the ubiquitin-like protein Nedd8 to protein targets, has recently emerged as a central and versatile regulator of many cellular processes, including gene transcription, metabolism, and cellular differentiation. In this study, we show that genetic and pharmacological inhibition of neddylation in vivo in developing Schwann cells lead to striking nerve defects that exhibit the classical hallmarks of a severe neuropathy, including gait abnormalities, muscle weakness, and hindlimb clasping, ultimately leading to early death. The mutant mice lack peripheral myelin and develop secondary axonal loss, and we demonstrate, at the mechanistic level, that neddylation regulates multiple critical myelination-related pathways. Together, our findings identify neddylation as a central regulatory hub of control of peripheral myelination and delineate the potential pathogenetic mechanisms in inherited human PNS disorders, characterized by mutations in genes related to the neddylation pathway.

2024-06-16 | PXD043917 | Pride

Evaluation of microRNA levels in recipient BMMSCs of MRL/lpr mice after cell therapy (miRNA)

Project description:Mesenchymal stem cell transplantation (MSCT) has been widely used to treat a variety of human diseases. However, the detailed mechanisms underlying its success are not fully understood. Here we show that MSCT rescues recipient bone marrow mesenchymal stem cell (BMMSC) function in Fas-deficient-MRL/lpr systemic lupus erythematosus (SLE) mice via a miR-29b/Dnmt1/Notch epigenetic cascade. Using the microRNA microarray, we found that MSCT could rescue the high level of miR-29b in the recipient BMMSCs of MRL/lpr mice. In the present study, mesenchymal stem cell transplantation (MSCT) was used to treat MRL/lpr mice. One week after the treatment, normal control MSCs from C3H/HeJ mice (C3H), recipient MSCs from untreated MRL/lpr mice (LPR) and recipient MSCs from MSCT-treated MRL/lpr mice (MSC) were used for total RNA extraction and microRNA microarray for analysis of microRNA expressions.

2014-03-20 | E-GEOD-55971 | biostudies-arrayexpress

Effect of LPS and the glucocorticoid dexamethasone on the mouse Bone Marrow Derived Macrophage Proteome

Project description:The concentrations and copy number of proteins in the mouse Bone Marrow Derived proteome was determined for control, 10 ng/mL LPS stimulation, and LPS stimulation plus the addition of 100 nM dexamethasone, after an incubation for 24 hours and with four biological replicates for each condition. Over 6000 proteins were detected, 410 of which were upregulated by LPS (> 1.5-fold increase, adjusted p value < 0.05). 125 of these LPS-induced proteins were significantly regulated by Dexamethason > 1.5 fold 899 increase or decrease, adjusted p value <0.05).

2024-01-26 | PXD041375 | 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