Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Inflammatory disease progression shapes nanoparticle biomolecular corona-mediated immune activation profiles

ABSTRACT: Polymeric nanoparticles (NPs) have emerged as promising tools for immunomodulation in various disease contexts. The interactions between the NP surface and plasma-resident biomolecules result in the formation of a biomolecular corona (BC), which varies patient-to-patient and as a function of disease state, resulting in the concept of the personalized NP-BC. This study investigates how the progression of systemic inflammatory disease influences the NP-BC composition and its corresponding effects on innate immune cell interactions and activation profiles. Employing a murine model of systemic inflammation, the dynamic changes in plasma biomolecule composition and their corresponding NP-BC fingerprints were elucidated. An integrated multi-omics approach was developed to reveal disease state-specific alterations in innate immune cell phenotypes and modulated signaling pathways to identify and confirm key circulating biomolecules that contribute to the dynamic immunostimulatory capabilities of BCs.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Mehari Weldemariam

LAB HEAD: Maureen Kane

PROVIDER: PXD050918 | Pride | 2025-01-17

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20221224_RyanLab_nanoparticle_mouse_serum_01.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_02.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_03.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_04.raw	Raw
	20221224_RyanLab_nanoparticle_mouse_serum_05.raw	Raw

Items per page:

1 - 5 of 21

Similar Datasets

Modulation of Pulmonary Toxicity in Metabolic Syndrome due to Variations in Nanoparticle-Biocorona Composition

Project description:Following introduction into a biological environment, nanoparticles (NPs) interact with biomolecules forming a biocorona (BC) on their surface altering cell interactions and toxicity. Metabolic syndrome (MetS) is a prevalent condition and enhances susceptibility to inhaled exposures. We hypothesize distinct NP-biomolecule interactions occur in the lungs due to MetS resulting in the formation of unique NP-BCs contributing to enhanced toxicity. Bronchoalveolar lavage fluid (BALF) was collected from healthy and MetS mouse models and used to evaluate variations in the BC formation on 20 nm iron oxide NPs. NPs without or with BCs were characterized for hydrodynamic size and zeta potential. Protein and lipid components of the BCs were evaluated via proteomic and lipidomic assessments. Unique biomolecules were determined to associate with iron oxide NPs while shared biomolecules demonstrated differential abundance based on disease state. A mouse macrophage cell line was utilized to examine alterations in cell interactions and toxicity due to BCs. Exposures for 1h or 24h with NPs did not demonstrate overt cytotoxicity. Darkfield microscopy and X-ray fluorescence (XRF) analysis determined enhanced iron oxide NP internalization due to the MetS BC compared to the healthy BC. Macrophages exposed to NPs with a MetS-BC for 1h or 24h demonstrated enhanced gene expression of inflammatory markers CCL2, IL-6, and TNF-alpha compared to ion oxide NPs with a healthy BC. Inflammatory pathways were examined by western blots to determine activation of specific proteins within the MAP kinase, Jak-Stat, and NF- kB signaling pathways. Activation of STAT3, NF-kB, and ERK pathways were determined to be upregulated due to the MetS-BC. Specifically, the Jak-Stat pathway was determined to be the most upregulated inflammatory pathway following exposure to NPs with a MetS BC.

2022-04-27 | MSV000089322 | MassIVE

caArray_geral-00143: An estrogen receptor-negative breast cancer subset characterized by a hormonally regulated transcriptional program and response to androgen

2015-05-15 | GSE68892 | GEO

caArray_geral-00143: An estrogen receptor-negative breast cancer subset characterized by a hormonally regulated transcriptional program and response to androgen

Project description:Clinical heterogeneity of esrtrogen receptor-negative, progesterone receptor-negative [ER(-)/PR(-)] breast cancer (BC) suggests biological heterogeneity. We performed gene expression analysis of primary BCs and BC cell lines to identify the underlying biology of ER(-)/PR(-) disease, define subsets, and identify potential therapeutic targets. geral-00143 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HG-U133A Organism: Homo sapiens (ncbitax) Material Types: cRNA, cell, OrganismPart, whole_organism, total_RNA Disease States: breast carcinomas

2015-05-15 | E-GEOD-68892 | biostudies-arrayexpress

Gene expression in mouse tracheal basal cells

2009-07-02 | GSE15724 | GEO

The TFIID subunit TAF4 is required for pancreatic beta cell function and identity [single-cell RNA-seq]

Project description:We selectively inactivated the Taf4 subunit of general transcription factor TFIID in adult murine pancreatic beta cells (BCs). Taf4 inactivation rapidly diminishes expression of critical genes involved in BC function leading to increased glycaemia, lowered blood insulin levels, defective glucose-stimulated insulin secretion and in the longer term reduced BC mass through apoptosis of a subpopulation of BCs. Nevertheless, glycaemia and blood insulin levels are stabilised after 11 weeks with mutant animals showing long term survival. Bulk RNA-seq and ATAC-seq and single cell RNA-seq on isolated Langerhans islets show that Taf4 loss leads to major remodelling of chromatin accessibility and gene expression not only in targeted BCs, but also alpha and delta cells. One week after Taf4-loss cells with mixed BC, alpha and/or delta cell identities were observed as well as a population trans-differentiating into alpha cells. Trans-differentiation was associated with the concerted action of the Mafb, Mafg, Bptf and Foxp1 transcription factors. Taf4 is therefore essential for BC function and identity and we identify a novel set of factors associated with BC trans-differentiation.

2021-06-01 | GSE151365 | GEO

The TFIID subunit TAF4 is required for pancreatic beta cell function and identity [RNA-seq]

2021-06-01 | GSE151364 | GEO

The TFIID subunit TAF4 is required for pancreatic beta cell function and identity [ATAC-seq]

2021-06-01 | GSE151363 | GEO

Exaggerated BMP4 signalling alters human airway basal progenitor cell differentiation to cigarette smoking-related phenotypes [array]

Project description:Airway remodelling in chronic obstructive pulmonary disease (COPD) originates, in part, from smoking-induced changes in airway basal stem/progenitor cells (BCs). Based on the knowledge that bone morphogenetic protein 4 (BMP4) influences epithelial progenitor function in the developing and adult mouse lung, we hypothesised that BMP4 signalling may regulate the biology of adult human airway BCs relevant to COPD. BMP4 signalling components in human airway epithelium were analysed at the mRNA and protein levels, and the differentiation of BCs was assessed using the BC expansion and air-liquid interface models in the absence/presence of BMP4, BMP receptor inhibitor and/or small interfering RNAs against BMP receptors and downstream signalling.

2020-05-28 | GSE128708 | GEO

Exaggerated BMP4 signalling alters human airway basal progenitor cell differentiation to cigarette smoking-related phenotypes [RNA-Seq]

2020-05-28 | GSE101353 | GEO

Transcription profiling of mouse tracheal basal cells

Project description:Epithelial basal cells (BCs) are an important stem cell population of the airways. We purified BCs from a KRT5-GFP transgenic mouse line and used Affymetrix arrays to compare there gene expression to that of non-BC epithelium. Experiment Overall Design: Three populations of cells were obtained by FACS: 1. KRT5-GFP-, lectin- columnar epithelium. 2. KRT5-GFP-, lectin+ BCs. 3. KRT5-GFP+, lectin+ BCs. Three biological replicates of each sample were hybridized to Affymetrix microarray.

2009-07-11 | E-GEOD-15724 | biostudies-arrayexpress

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