Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Targeted immunotherapy rescues pulmonary fibrosis by reducing activated fibroblasts and regulating alveolar cell profile

ABSTRACT: Targeted immunotherapy rescues pulmonary fibrosis by reducing activated fibroblasts and regulating alveolar cell profile

PROVIDER: PRJNA1192992 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31567286_1.fastq.gz	Fastqsanger.gz
	SRR31567286_2.fastq.gz	Fastqsanger.gz
	SRR31567287_1.fastq.gz	Fastqsanger.gz
	SRR31567287_2.fastq.gz	Fastqsanger.gz
	SRR31567288_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Targeted immunotherapy rescues pulmonary fibrosis by reducing activated fibroblasts and regulating alveolar cell profile

Project description:Idiopathic pulmonary fibrosis (IPF) is a severe lung disease in the world, but has limited clinical therapies. Fibrosis maintains dynamic balance with overactivated fibroblasts. Given pulmonary cell regeneration, the lung may have self-repairing ability if fibrosis is removed by clearance of overactivated fibroblasts. The aim of the study is to evaluate therapeutic activity of transient CAR-T cells generated via a novelly designed LNP-mRNA system and address the relevant mechanism to epithelial cell polarization in a mouse model of bleomycin-induced IPF. Studies on proteomes and histology showed that fibrosis-induced ECM stiffening impaired epithelial cell polarization that limited cell’s self-healing ability. The proposed LNP-mRNA therapy eliminated overactivated fibroblasts and removed pulmonary fibrosis successfully. The decreased ECM stiffness and the improvement of extracellular environment facilitated re-establishment of cell polarity and restored the self-repairing ability of epithelial cell. Hence, LNP-mRNA treatment for IPF can recover pulmonary structure and function close to a healthy lung. This therapy shows a potential treatment for IPF patients.

2025-03-19 | PXD053333 | Pride

Targeted immunotherapy rescues pulmonary fibrosis by reducing activated fibroblasts and regulating alveolar cell profile

Project description:The single-cell RNA-seq libraries were generated with 10x genomics from mouse lungs. Model mice were treated with saline (n=2) or transient CAR-T cells generated by LNP in vivo (n=2) after bleomycin-induced injury. The samples were taken at day28 after surgery and collected as the fresh whole lung tissue.

2025-03-19 | GSE283267 | GEO

Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy

Project description:Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy

| PRJNA786531 | ENA

Proteomics of Pulmonary alveolar microlithiasis nodules

Project description:The proteomics aspect of this project was simply to catalog the protein content in microlith nodule isolated from a Pulmonary alveolar microlithiasis patient or from a mouse model of the disease

2023-03-11 | PXD039280 | Pride

Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis

Project description:Pulmonary alveolar microlithiasis is an autosomal recessive lung disease caused by a deficiency in the pulmonary epithelial Npt2b sodium-phosphate co-transporter that results in accumulation of phosphate and formation of hydroxyapatite microliths in the alveolar space. The single cell transcriptomic analysis of a pulmonary alveolar microlithiasis lung explant showing a robust osteoclast gene signature in alveolar monocytes and the finding that calcium phosphate microliths contain a rich protein and lipid matrix that includes bone resorbing osteoclast enzymes and other proteins suggested a role for osteoclast-like cells in the host response to microliths. While investigating the mechanisms of microlith clearance, we found that Npt2b modulates pulmonary phosphate homeostasis through effects on alternative phosphate transporter activity and alveolar osteoprotegerin, and that microliths induce osteoclast formation and activation in a receptor activator of nuclear factor kappa B (NF-kB) ligand and dietary phosphate dependent manner. This work reveals that Npt2b and pulmonary osteoclast like cells play key roles in pulmonary homeostasis and suggest potential new therapeutic targets for the treatment of lung disease.

2023-02-16 | MSV000091302 | MassIVE

Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy - Targeted Pooled CRISPR Screen for T cell Exhaustion

Project description:Targeting SNX9 rescues CD28-mediated T cell exhaustion for cancer immunotherapy - Targeted Pooled CRISPR Screen for T cell Exhaustion

| PRJNA786536 | ENA

GNPS - Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis

2023-02-16 | MSV000091302 | GNPS

Targeted alveolar regeneration with Frizzled-specific agonists

Project description:Wnt ligands oligomerize Frizzled (Fzd) and Lrp5/6 receptors to control the specification and activity of stem cells in many species. How Wnt is selectively activated in different stem cell populations, often within the same organ, is not understood. In lung alveoli, wherein Wnt-dependent epithelial and stromal progenitors are intermingled, we show that distinct Wnt receptors are expressed by epithelial (Fzd5/6), endothelial (Fzd4), and stromal (Fzd1) cells. Moreover, Fzd5 was uniquely required for alveolar epithelial stem cell activity. However, by developing an expanded repertoire of Fzd-Lrp agonists (FLAgs), we could activate canonical Wnt signaling in alveolar epithelial stem cells via either Fzd5 or, unexpectedly, non-canonical Fzd6. Fzd5 and Fzd6 FLAgs stimulated supra-physiological alveolar epithelial stem cell activity in mice following lung injury, but only Fzd6 FLAg promoted an alveolar fate in airway-derived progenitors. Therefore, we identify a potential strategy for promoting regeneration without exacerbating fibrosis during lung injury.

2023-06-16 | GSE208770 | GEO

citrate vs nitrate Reducing cultures

Project description:The effect of nitrate reduction (anaerobic cultivation in the presence of heme, vitamin K2 and nitrate) was compared with anaerobic cultivation supplemented with citrate (Lactobacillus plantarum). The medium was chemically defined medium with mannitol as main carbon source Two-condition experiment, nitrate vs citrate reducing cells. Biological replicates: 4 nitrate reducing cultures, 4 citrate reducing cultures, independently grown and harvested. Two slides were used, each slide contained 8 Arrays. Citrate reducing cultures are called reactor 1-4, Nitrate reducing cultures are called reactor A-D

2010-05-16 | E-GEOD-18339 | biostudies-arrayexpress

Activation of SREBP in Alveolar Type II Cells Enhances Lipogenesis Causing Pulmonary Lipotoxicity

Project description:Background: Lung function is dependent upon the precise regulation of the synthesis, storage, and catabolism of tissue and alveolar lipids. Results: Activation of SREBP (Sterol Response Element Binding Protein) induced lipogenesis in alveolar epithelial cells, causing neutral lipid accumulation, lung inflammation, and tissue remodeling. Conclusions: The accumulation of neutral lipids in type II epithelial cells and alveolar macrophages caused lung inflammation, consistent with findings in lipid storage disorders. Significance: Pulmonary lipotoxicity may contribute to the pathogenesis of lung dysfunction associated with diabetes, obesity, and other metabolic disorders. Genome-wide transcription profiling comparison between doxycycline-exposed SFTPC-rtTAWT/Tg/(tetO)7CMV-CreWT/Tg/Insig1flox/flox/Insig2-/- mice (i.e., Insig1/2∆/∆ ) and Insig1flox/flox/Insig2-/- . Three independent pooled RNA from isolated lung type 2 cells of each genotype were used.

2012-03-01 | E-GEOD-31797 | 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