Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MicroRNA expression profiles of extracellular vehicles released from alveolar macrophage

ABSTRACT: microRNA expression profiles of extracellular vehicles released from alveolar macrophage

PROVIDER: PRJNA763370 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15902444.fastq.gz	Fastqsanger.gz
	SRR15902445.fastq.gz	Fastqsanger.gz
	SRR15902446.fastq.gz	Fastqsanger.gz
	SRR15902447.fastq.gz	Fastqsanger.gz
	SRR15902448.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

microRNA expression profiles of extracellular vehicles released from alveolar macrophage

Project description:Interstitial lung diseases (ILDs) such as idiopathic pulmonary fibrosis (IPF) is diffuse parenchymal lung disorders characterized by varying degrees of inflammation and fibrosis of the lung interstitium. The failure of lung alveolar regeneration in IPF is critical for this incurable disease. Here we report that chronic lung injury causes a profibrotic phenotype of alveolar macrophages that release extracellular vehicles (EVs) to promote PF development through repressing the stemness traits of type 2 alveolar epithelial cells (AEC2s). We found that an increased expression of acetylases KAT5 interacts with and acetylates protein kinase MLKL, which directly promotes release of EVs from AMs following chronic lung injury. AEC2s takes up the EVs and releases miR-148a-3p to repress expression of endogenous b-catennin agonist Wnt10b and alveolar regeneration. Pharmacologic inhibition of the miR-148a-3p expression or interruption of the KAT5-MLKL interaction restores regenerative capacity of AEC2s and exhibits potent therapeutic efficacy against PF. Our study confers a potential strategy for the treatment of IPF and other interstitial lung diseases.

2023-09-01 | GSE184147 | GEO

Cigarette smoke extract-treated alveolar macrophage-derived extracellular vesicles

Project description:This project is based upon the fundamental observation that alveolar macrophage-derived extracellular vesicles (AM-EVs), when internalized by neighboring epithelial cells, inhibit their infection by influenza virus. This inhibitory activity of AM-EVs is abolished when AMs are treated with cigarette smoke extract (CSE). We chose to survey the AM-EV proteome in an effort to identify candidate proteins whose abundance within EVs was downregulated by CSE treatment of AMs, thus explaining the ability of CSE to abrogate the inhibitory activity against influenza.

2020-06-09 | PXD019528 | Pride

The transcriptional response of Trichomonas vaginalis to Trichomonas-derived extracellular vehicles

Project description:The transcriptional response of Trichomonas vaginalis to Trichomonas-derived extracellular vehicles

| PRJNA1066203 | ENA

The transcriptional response of prostate cells to Trichomonas vaginalis extracellular vehicles

Project description:The transcriptional response of prostate cells to Trichomonas vaginalis extracellular vehicles

| PRJNA1166875 | ENA

Alveolar macrophage gene expression - PIKfyve knockout

Project description:comparison of Alveolar macrophge gene expression in wild type and PIKfyve ko We identifed gene that important for alveolar macrophage development

2017-03-01 | GSE93849 | GEO

Cytomegalovirus subverts macrophage identity [Alveolar macrophages]

Project description:Cytomegalovirus subverts macrophage identity [Alveolar macrophages]

| PRJNA668753 | ENA

CD11b restricts alveolar macrophage activation during pneumococcal pneumonia and prevents excessive lung inflammation

Project description:Bacterial lung infections are associated with strong infiltration of CD11b+ myeloid cells, which limit life-threatening disease, but also severely damage lung tissue. In a murine lung infection model with Streptococcus pneumoniae, we found intrinsic upregulation of CD11b on resident alveolar macrophages. Such CD11b expression was associated with transcriptomic and proteomic adaptations by alveolar macrophages, leading to the identification of specific molecules and pathways that depended on CD11b. In the absence of CD11b, the antimicrobial defense of alveolar macrophages was strongly reduced, and the production of neutrophil-recruiting chemokines was more pronounced. Moreover, CD11b expression limited the infection and prevented excessive alveolar damage. In conclusion, our study provides detailed molecular insights into the alveolar macrophage-specific immune response to Streptococcus pneumoniae lung infection and reveals profound CD11b-dependent alterations that are critical for effective antimicrobial immunity, neutrophil recruitment, and prevention of alveolar damage.

2023-10-08 | PXD035269 | Pride

Macrophage response to extracellular ADP stimulation

Project description:Macrophage response to extracellular ADP stimulation

| PRJNA644410 | ENA

Extracellular vesicle labeled Granulocyte macrophage progenitors

Project description:Extracellular vesicle labeled Granulocyte macrophage progenitors

| PRJNA525660 | ENA

The Aging Microenvironment Drives Alveolar Macrophage Changes in Aging [RNA-Seq]

Project description:Our study shows that the aging lung microenvironment shapes the transcriptional phenotype of alveolar macrophages during aging. Except during acute injury when alveolar macrophage differentiation is incomplete, cellular ontogeny makes little difference in determining the transcriptional response of alveolar macrophages. Studies with parabiosis suggest the age-related changes in the alveolar microenvironment occur independently of circulating factors or cells. Our findings suggest that changes that target the microenvironment, for example metformin, senolytics or others might indirectly improve macrophage function during aging.

2020-12-31 | GSE134397 | GEO

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