Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

ABSTRACT: Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

PROVIDER: PRJNA1050154 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27144229_1.fastq.gz	Fastqsanger.gz
	SRR27144229_2.fastq.gz	Fastqsanger.gz
	SRR27144230_1.fastq.gz	Fastqsanger.gz
	SRR27144230_2.fastq.gz	Fastqsanger.gz
	SRR27144231_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

Project description:Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

| PRJNA1234675 | ENA

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

Project description:Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

| PRJNA1214361 | ENA

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

Project description:Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the pathological effects of type I interferon (IFN-I) during infection and damage in mice. At baseline, OSM-deficient mice exhibited altered alveolar type II (ATII) epithelial cell states. In response to influenza or viral mimic challenge, mice lacking OSM exhibited heightened IFN-I responses and increased mortality. Furthermore, OSM promoted organoid formation despite the growth-inhibitory effects of IFN-I. These findings identify OSM as an indispensable macrophage-derived growth factor that maintains the homeostasis of lung epithelial cells and promotes their proliferation to overcome IFN-I-mediated immunopathology.

2025-07-10 | GSE287742 | GEO

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

2023-12-15 | GSE249668 | GEO

Macrophage-derived oncostatin M repairs the lung epithelial barrier during inflammatory damage

Project description:Tissue repair programs must function alongside antiviral immunity to restore the lung epithelial barrier following infection. We found that macrophage-derived oncostatin M (OSM) counteracted the pathological effects of type I interferon (IFN- I) during infection and damage in mice. At baseline, OSM-deficient mice exhibited altered alveolar type II (ATII) epithelial cell states. In response to influenza or viral mimic challenge, mice lacking OSM exhibited heightened IFN-I responses and increased mortality. OSM delivery to the lung induced ATII proliferation and was sufficient to protect deficient mice against morbidity. Furthermore, OSM promoted organoid formation despite the growth- inhibitory effects of IFN- I. These findings identify OSM as an indispensable macrophage-derived growth factor that maintains the homeostasis of lung epithelial cells and promotes their proliferation to overcome IFN-I–mediated immunopathology.

2025-07-10 | GSE291698 | GEO

neonatal rat cardiomyocytes stimulated by Oncostatin M

Project description:Molecular analysis of transcriptional changes in cardiomyocytes induced by Oncostatin M treatment. The rationale of this experiment is described in [Kubin, T., et al. Oncostatin M is a major mediator of cardiomyocyte dedifferentiation and remodeling. Cell stem cell 9, 420-432 (2011)]

2015-02-27 | E-MTAB-2560 | biostudies-arrayexpress

High glucose levels increase influenza-associated damage to the pulmonary epithelial-endothelial barrier

Project description:Here, the effects of high glucose levels on influenza severity were investigated using an in vitro model of the pulmonary epithelial-endothelial barrier. We show that compared to low glucose levels, high glucose conditions prior to influenza A virus infection increased virus-induced barrier damage. Increased barrier damage was not associated with increased cell death nor increased virus replication, but rather an increased pro-inflammatory response in endothelial cells and the subsequent damage of the epithelial junctional complex.

2020-02-14 | GSE145232 | GEO

Antibiotics damage the colonic mucus barrier in a microbiota-independent manner

Project description:Antibiotics damage the colonic mucus barrier in a microbiota-independent manner

| PRJNA1126684 | ENA

Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

Project description:Gut epithelial barrier damage caused by dishwasher detergents and rinse aids

| PRJNA841364 | ENA

Exercise-induced Crosstalk between Immune Cells and Adipocytes in Humans: Role of Oncostatin-M

Project description:The discovery of novel exercise-regulated circulatory factors has fueled interest in the role of organ-crosstalk, especially between skeletal muscle and adipose tissue in mediating beneficial effects of exercise. We studied the adipose tissue transcriptome in men and women with normal glucose tolerance or type 2 diabetes following an acute exercise bout, revealing substantial exercise and time-dependent changes, and a sustained increase in inflammatory genes unique to Type 2 diabetes. We identify Oncostatin-M as one of the most upregulated adipose tissue secreted factors post exercise. In cultured human adipocytes, oncostatin-M enhanced MAPK signalling and regulates lipolysis. Oncostatin-M expression predominantly arises from adipose tissue immune cell fractions, while the corresponding receptors are expressed in adipocytes. Oncostatin-M expression is induced in cultured human Thp1 macrophages in response to exercise-like stimuli. Our results suggest immune cells, via secreted factors such as oncostatin-M, are important in crosstalk between skeletal muscle and adipose tissue during exercise, to regulate adipocyte metabolism and adaptation.

2023-11-21 | GSE198922 | 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