Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Determining the impact of anti-IL6 and anti-OSM on macrophage and fibroblast biology in a model of fibrotic lung disease [NGS3341]

ABSTRACT: To determine the comparative effect of anti-IL6 and anti-OSM treatment in lung fibrosis, mice received saline or bleomycin via instillation and then received antibodies via intraperitoneal injection once weekly until take down. At day 14, mice were euthanized, lungs were isolated and lysed in RLT buffer. Total RNA was extracted and sequenced by bulk RNA-sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE262966 | GEO | 2026/01/06

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Determining the impact of anti-IL6 and anti-OSM on macrophage and fibroblast biology in a model of fibrotic lung disease [NGS3341]

Project description:Determining the impact of anti-IL6 and anti-OSM on macrophage and fibroblast biology in a model of fibrotic lung disease [NGS3341]

| PRJNA1095009 | ENA

Gene expression of HCT116 cells after stimulation with oncostatin M (OSM)

Project description:To evaluate gene expression profiles in intestinal epithelial cells (IEC) after OSM stimulation, we have employed whole genome microarray expression profiling as a discovery platform to identify relevant genes which are potentially of interest to reveal the role of OSM in intestinal inflammation. The most strongly up-regulated genes were SERPINS, which belong to the family of serin peptidase inhibitors with antiprotease activities, most of them serine and cysteine proteases. SERPINB4, SERPINB3 and SERPINA3 were the genes with the strongest up-regulation, also verified in qPCR. OSM-induced SERPIN up-regulation may contribute to anti-apoptotic and proliferative effects of OSM in IEC. HCT116 cells were starved overnight with medium containing 1% FCS after reaching 70% confluency. On the next day, cells were stimulated in quadruplicates with 100 ng/mL OSM or left unstimulated. RNA was isolated 6 hours after stimulation and RNA concentration and purity was measured.

2014-12-13 | E-GEOD-53295 | biostudies-arrayexpress

Gene expression of HCT116 cells after stimulation with oncostatin M (OSM)

2014-12-13 | GSE53295 | GEO

Oncostatin M (OSM) and Leukemia Inhibitory factor (LIF) treatment of osteoblasts via LIF and OSM receptors

Project description:Oncostatin M (OSM) and Leukemia Inhibitory Factor (LIF) signal within cells via the gp130 (Il6st) coreceptor bound either to the LIF receptor (LIFR) or the oncostatin M receptor (OSMR), but whether murine OSM can act through both receptors is controversial. Both LIF and OSM stimulate bone formation, inhibit adipocyte differentiation, and promote osteoclast differentiation, but our earlier work suggested this may depend on the receptor subtype used. This project aimed to identify those gene targets regulated by murine OSM via OSMR and LIFR by using wild type and OSMR null primary osteoblasts. Cells were differentiated to their most mature state (i.e. osteocytes) because the only prior target gene known to be regulated by murine OSM via the LIFR was an osteocyte-specific gene, sclerostin.

2016-08-17 | GSE83418 | GEO

Heterocellular OSM-OSMR signalling drives pancreatic tumour growth and metastasis through functional fibroblast reprogramming

Project description:Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy characterised by a pathologicalfibroinflammatorymicroenvironment. Dichotomous tumour-promoting and -restrictive roles have been ascribed to the tumour microenvironment, however thedisparate effect of individual stromal subsets remains incompletely characterised. Here, we describe how heterocellular OSM-OSMR signalling instructsfibroblast reprogramming,tumourgrowth and metastasis.Macrophage-secreted OSM stimulatesinflammatory gene expression in cancer-associated fibroblasts (CAFs), which in turn induce a pro-tumorigenic environment and engage tumour cellsurvival and migratory signalling pathways. Tumour cells implanted in Osm-deficient (Osm-/-) mice display an epithelial-dominated morphology, reduced tumour growth and did notmetastasise. Moreover, the tumour microenvironment of Osm-/-animals exhibit increased abundance of αSMAposmyofibroblasts and a shift in myeloid and T cell phenotypes, consistent with a more immunogenic environment. Taken together, these data demonstrate how OSM-OSMR signalling coordinates heterocellular interactions to drive a pro-tumorigenic environment in PDA.

2021-11-29 | PXD022484 | Pride

Crotamiton derivative JM03 extends lifespan and improves oxidative and hypertonic stress resistance in Caenorhabditis elegans via inhibiting OSM-9

Project description:While screening our in-house 1,072 marketed drugs for their ability to extend the lifespan using Caenorhabditis elegans (C. elegans) as an animal model, crotamiton (N-ethyl-o-crotonotoluidide) showed anti-aging activity and was selected for further structural optimization. After replacing the ortho-methyl of crotamiton with ortho-fluoro, crotamiton derivative JM03 was obtained and showed better activity in terms of lifespan-extension and stress resistance than crotamiton. It was further explored that JM03 extended the lifespan of C. elegans through osmotic avoidance abnormal-9 (OSM-9). Besides, JM03 improves the ability of nematode to resist oxidative stress and hypertonic stress through OSM-9, but not osm-9/capsaicin receptor related-2 (OCR-2). Then the inhibition of OSM-9 by JM03 reduces the aggregation of Q35 in C. elegans via upregulating the genes associated with proteostasis. SKN-1 signaling was also found to be activated after JM03 treatment, which might contribute to proteostasis, stress resistance and lifespan extension. In summary, this study explored a new small molecule derived from crotamiton, which has efficient anti-oxidative, anti-hypertonic and anti-aging effects, and could further lead to promising application prospects.

2022-04-10 | GSE200459 | GEO

Expression data from cancer associated fibroblasts (CAFs) treated with OSM

Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in CAFs, a small and well-annotated Clariom S gene microarray was performed in CAF-173 cells cultured in 3D spheroids and treated with OSM or vehicle (PBS).

2022-02-02 | GSE195775 | GEO

Microarray analysis of Huh7 cells treated with IFNa2, OSM or IFNa2 combined with OSM

Project description:OSM increases the antiviral effect of IFNα in Huh7 cells infected with hepatitis A virus (HAV) or HCV replicon and synergizes with IFNα in the induction of antiviral genes 16 samples. Four replicates for each experimental condition. 72 hours of treatment in DMEM supplemented with 2% FBS.

2009-01-20 | E-GEOD-13046 | biostudies-arrayexpress

Crotamiton derivative JM03 extends lifespan and improves 1 oxidative and hypertonic stress resistance in Caenorhabditis 2 elegans via inhibiting OSM-9

2021-09-17 | GSE184076 | GEO

Response of several cell lines originated from liver, skin and colon to stimulation by IFNg, hyper-IL6, IL27 and OSM, investigated at mRNA level

Project description:In this study 6 cell lines originated from liver, skin and colon tumours as well as 3 non-tumour cell lines from the same organs were profiled with and without stimulation by 4 cytokines: IFNg, hyper-IL6, IL27 and OSM. The main objective was investigation of downstream effects of the stimulation if these cancer cell lines as well as in healthy tissues.

2018-10-01 | E-MTAB-6080 | 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