Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Multiplexed quantitative proteomics in a pig model of aging

ABSTRACT: Characterization of the heart proteome in a pig model of aging

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Sus Scrofa Domesticus (domestic Pig)

TISSUE(S): Heart

SUBMITTER: Inmaculada Jorge

LAB HEAD: Jesús Vázquez Cobos

PROVIDER: PXD019532 | Pride | 2020-12-01

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Prog_pig_1-10_8ug.msf	Msf
	Prog_pig_1-10_8ug.raw	Raw
	Prog_pig_1-10_8ug_ii.msf	Msf
	Prog_pig_1-10_8ug_ii.raw	Raw
	Prog_pig_1-10_HpH_1.msf	Msf

Items per page:

1 - 5 of 24

Publications

Identification of common cardiometabolic alterations and deregulated pathways in mouse and pig models of aging.

Fanjul Víctor V Jorge Inmaculada I Camafeita Emilio E Macías Álvaro Á González-Gómez Cristina C Barettino Ana A Dorado Beatriz B Andrés-Manzano María Jesús MJ Rivera-Torres José J Vázquez Jesús J López-Otín Carlos C Andrés Vicente V

Aging cell 20200730 9

Aging is the main risk factor for cardiovascular and metabolic diseases, which have become a global concern as the world population ages. These diseases and the aging process are exacerbated in Hutchinson-Gilford progeria syndrome (HGPS or progeria). Here, we evaluated the cardiometabolic disease in animal models of premature and normal aging with the aim of identifying alterations that are shared or specific to each condition. Despite differences in body composition and metabolic markers, prema ...[more]

PMID: 32729659

Similar Datasets

Multiplexed quantitative proteomics in mouse model of aging

Project description:Characterization of the heart proteome in a mouse model of aging

2020-12-01 | PXD019533 | Pride

p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia

Project description:Ventricular fibrillation (VF) is a leading immediate cause of sudden cardiac death. There is a strong association between aging and VF, although the mechanisms are unclear, limiting the availability of targeted therapeutic interventions. Here we found find that the stress kinases p38 and p38/are activated in the ventricles of old mice and mice with genetic or drug-induced arrhythmogenic conditions. We discovered that upon activation, the increased activity of p38 and p38/ was cooperatively associated increase the with susceptibility to stress-induced VF. Mechanistically, our data indicate that activated p38 and p38wphosphorylatee identified ryanodine receptor 2 (RyR2) and disrupt Kv4.3 channel localization, as a new substrate of p38/. Our data indicate that phosphorylation of SAP97 by activated p38/ also disrupts Kv4.3 localization at the plasma membrane, promoting sarcoplasmic reticulum calcium leak, Ito current reduction and action potential duration prolongation. In turn, this led to aberrant intracellular calcium handling, premature ventricular complexes, and enhanced susceptibility to VF. The importance of this finding is evidenced by the fact that bBlocking this pathway protected genetically modified animals from VF development and reduced the VF duration in aged animals. We have identified p38/-driven phosphorylation of RyR2 and SAP97 as a novel trigger of VF. These results indicate that p38 and p38/ are a new potential therapeutic target for sustained VF prevention.

2023-10-18 | PXD045996 | Pride

Aging induces hepatic oxidative stress and nuclear proteomic remodelling in liver from Wistar ratAging induces hepatic oxidative stress and nuclear proteomic remodelling in liver from Wistar rats

Project description:Aging induces oxidative stress and proteome remodeling in the nucleus from liver in Wistar rats

2022-02-17 | PXD027773 | Pride

Diferential expression analyses PLAC8 defective cells

Project description:SARS-CoV-2 pandemic has caused a dramatic health, social and economic crisis worldwide. To better understand the host-virus interactions and identify potentially targetable host factors, we have conducted CRISPR-Cas9 genetic screens using SARS-CoV-2 pseudotyped lentiviruses on human lung cancer cells. Our results recapitulate many findings from previous screens that used full SARS-CoV-2 viruses, but also unveil two novel critical host factors: SPNS1 and PLAC8. Functional experiments with full SARS-CoV-2 viruses have confirmed that loss-of-function of these genes impairs viral entry. Importantly, we have found that PLAC8 is a key limiting host factor whose overexpression boosts viral infection in eight different human lung cancer cell lines. Using single-cell RNA-Seq data analyses, we demonstrate that PLAC8 is highly expressed in ciliated and secretory cells from the respiratory tract and in gut enterocytes, cell types that are highly susceptible to SARS-CoV-2 infection. Finally, proteomics and cell biology studies suggest that SPNS1 and PLAC8 affect viral entry through regulation of autophagy and lysosomal function.

2022-09-06 | PXD036334 | Pride

Multiplexed quantitative proteomics in an autoimmune mice model of myocarditis (EAM)

Project description:We performed a high-throughput, multiplexed quantitative proteomics analysis to determine protein abundance changes produced by BML-111 treatment in EAM and Ctrl mice. EAM was induced in 7 weeks-old BALB/c female mice by immunization at days 0 and 7 with a subcutaneous injection of 350 μg of murine cardiac myosin (MyHCα) in a 1:1 emulsion with complete Freund’s Adjuvant (SIGMA). MyHCα was isolated from hearts of Balb/c mice; control mice were injected with a 1:1 emulsion of physiological saline solution with complete Freund’s Adjuvant. Mice were treated daily for two weeks from day 7 by intraperitoneal injection with two complementary treatments: 1mg/Kg BML-111(Enzo Life Science) or its vehicle (2.5% ethanol). The proteomics analysis was performed in heart tissue protein extracts (four animals per group: Ctrl+Veh, EAM+Veh, Ctrl+BML and EAM+BML.

2022-12-07 | PXD024345 | Pride

Extracellular vesicles (EV) from IFNγ-primed cardiosphere-derived cells (CDCs)

Project description:Characterization of proteins in extracellular vesicles (EV) from cardiosphere-derived cells (CDCs) of a clinically relevant pig model. Additionally, considering that priming stem cells with inflammatory stimuli may increase the therapeutic potential of released vesicles, here we studied the dynamic changes that take place in the EV from IFNγ-primed CDCs.

2020-05-15 | PXD016434 | Pride

Multiplexed quantitative proteomics of extracellular vesicles released by endMSCs (EV-endMSCs)

Project description:The extracellular vesicles released by endMSCs (EV-endMSCs)were characterized by multiplexedquantitative proteomics approach. We hypothesized that inflammatory priming of adult stem cells may contribute to increase their therapeutic effectiveness, thus, extracellular vesicles derived from IFN-γ-primed endMSCs (IFNγ/EV-endMSCs) were compared to control counterparts (n=3 patients).

2019-12-17 | PXD015465 | Pride

Dll4iDEC mouse liver endothelial cells

Project description:Myc and its target Odc1 were among the most 250 strongly upregulated genes in Dll4 mutant ECs, compared with Notch1 and Rbpj mutants. Myc is known to activate important ribosome biogenesis and protein translation pathways, favoring cell growth. Dll4iDEC livers showed upregulation of a large range of canonical E2F, Myc, and mTORC1 target genes and ribosomal genes, particularly in the activated, proliferating, and endothelial tip-cell clusters. This hypermetabolic transcriptional status was confirmed by in-depth proteomics analysis of protein lysates obtained from freshly isolated liver ECs, providing the first proteomics analysis of the endothelial tip-cell state induced by targeting Dll4.

2023-04-11 | PXD041349 | Pride

Altered porcine PBMC proteome and secretome after stimulation with BanLec

Project description:With this experiment, we aimed at showing changes in the proteome and secretome of porcine peripheral blood mononuclear cells (PBMC) after stimulation with Banana Lectin (BanLec).

2021-08-26 | PXD027505 | Pride

Multiplexed quantitative proteomics of CD4 T cell-mediated postsynaptic dendritic cells (DC)

Project description:We aimed to characterize the proteome remodeling in DCs induced upon antigen presentation. To do so, we used an in vitro antigen presentation model to generate postsynaptic (psDC) or nonsynaptic (nsDC) DCs similarly to previously reported (Alcaraz-Serna et al., 2021). Bone marrow-derived DCs (BMDCs), which had been activated with LPS and pulsed (psDC) or not (nsDC) with the ovalbumin peptide OVA323-339, were co-cultured with resting CD4+ T cells from OT-II mice to allow cognate antigen-dependent immune synapse formation (psDC) or not (nsDC). DCs were then purified for proteomic analysis by using mass spectrometry based on multiplexed isotopic labeling peptides approach.

2024-01-26 | PXD039035 | 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