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Transcriptome profiling of murine cardiomyocytes after treatment with recombinant murine Leukemia inhibitory factor (mLIF), murine Oncostatin M (mOSM) and human-like Oncostatin M orthologue (hlOSM).

ABSTRACT: Transcriptome profiling of murine cardiomyocytes after treatment with recombinant murine Leukemia inhibitory factor (mLIF), murine Oncostatin M (mOSM) and human-like Oncostatin M orthologue (hlOSM).

PROVIDER: PRJNA768479 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16201267.fastq.gz	Fastqsanger.gz
	SRR16201268.fastq.gz	Fastqsanger.gz
	SRR16201269.fastq.gz	Fastqsanger.gz
	SRR16201270.fastq.gz	Fastqsanger.gz
	SRR16201271.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of murine cardiomyocytes after treatment with recombinant murine Leukemia inhibitory factor (mLIF), murine Oncostatin M (mOSM) and human-like Oncostatin M orthologue (hlOSM).

Project description:This study comparatively assesses downstream effects of exclusive activation of Leukemia inhibitory factor receptor (LIFR), Oncostatin M receptor (OSMR) and dual LIFR/OSMR signaling in murine, cultured cardiomyocytes upon administration of recombinant mLIF, mOSM and hlOSM that is capable to activate both receptors in murine cells.

2022-01-19 | GSE185305 | 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

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

Oncostatin M Regulation of Gene Expression in Breast Tumour Cells.

Project description:Oncostatin m (OSM) induces potent growth inhibitory and morphogenic responses in several different tumour cell types but the genetic events are not well understood. OSM can signal through two separate heterodimeric receptor complexes, gp130/LIFRα and gp130/OSMRβ. In this investigation we utilised cytokines, oncostatin M, interleukin-6 (IL-6) and leukaemia inhibitory factor (LIF) and LIF receptor antagonist, LIF-05, to help identify patterns of gene expression elicited by the different IL-6 receptor complexes in breast tumour cell line, T47D . We have tried to identify an OSM gene signature common to multiple breast tumour-derived cell lines (T47D, MCF-7 and MDA-MB-231) and identified OSM-gene regulation at time-points which coincide with the onset of OSM-induced biological effects. These findings identify a core transcriptional mechanism specific to the OSMRβ in breast tumour cells. Keywords: Comparative, timecourse, cell line-specific

2006-08-01 | GSE4661 | GEO

Effects of murine Oncostatin M on OP9 stromal cells and NIH/3T3 fibroblasts

Project description:The IL-6 cytokine Oncostatin M (OSM) is involved in cell development, growth, hematopoiesis, inflammation and cancer. Intriguingly, OSM has proliferative and antiproliferative effects de-pending on the target cell. The molecular mechanisms underlying these opposing effects are not fully understood and its role in tumorigenesis remains controversial. In the present study, we investigated the effect of murine OSM (mOSM) on proliferation in two cell types of distinct origin. We found that mOSM impairs the proliferation of murine bone marrow (BM) stromal cell lines and primary BM stromal cells, whereas murine fibroblasts responded to mOSM with increased proliferation. When we set out to reveal the mechanisms underlying these opposing effects of OSM on proliferation, we detected increased expression of the OSM receptors OSMR and LIFR in stromal cells. Interestingly, Osmr knockdown and Lifr overexpression attenuated the OSM-mediated effect on proliferation in both cell lines indicating that mOSM affected the pro-liferation of both cell lines signaling mainly through the OSMR. Furthermore, mOSM induced activation of the JAK-STAT, PI3K-AKT and MAPK-ERK pathways in OP9 and NIH/3T3 cells with differences in total protein levels between the two cell lines. Our findings offer new insights into the regulation of proliferation by mOSM.

2021-10-13 | GSE185646 | GEO

Effects of murine Oncostatin M on OP9 stromal cells and NIH/3T3 fibroblasts

Project description:Effects of murine Oncostatin M on OP9 stromal cells and NIH/3T3 fibroblasts

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Oncostatin M signaling drives cancer-associated skeletal muscle wasting

Project description:Investigating muscle wasting in a murine model of cancer cachexia, we identified Oncostatin M (OSM) as a potential mediator of inflammatory responses in skeletal muscle. OSM is a member of the IL-6 family of cytokines and has crucial functions in cell growth, differentiation, and inflammation. Our results demonstrate that OSM induces muscle atrophy. To understand if its effect is specific or it is a general effect of IL6 family cytokines, primary myotubes were treated with OSM, IL6 and LIF for 48hrs. Our findings showed that OSM potently induces muscle wasting in differentiated myotubes.

2024-03-21 | GSE222208 | GEO

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

Gain of the oncostatin M receptor in cervical squamous cell carcinoma is associated with adverse clinical outcome

Project description:This SuperSeries is composed of the following subset Series: GSE27331: Gain of the oncostatin M receptor in cervical squamous cell carcinoma is associated with adverse clinical outcome [penn1Mb data] GSE27332: Gain of the oncostatin M receptor in cervical squamous cell carcinoma is associated with adverse clinical outcome [camb1Mb data] GSE27673: An integrated genomics approach for novel biomarker discovery in squamous cell cervical carcinoma Refer to individual Series

2011-02-16 | E-GEOD-27333 | biostudies-arrayexpress

Oncostatin M effects in IMR90 cells

Project description:The JAK2 mutation V617F is detectable in a majority of patients with Ph-negative myeloproliferative neoplasms (MPN). Enforced expression of JAK2 V617F in mice induces myeloproliferation and bone marrow (BM) fibrosis suggesting a causal role for the JAK2 mutant in the pathogenesis of MPN. However, little is known about mechanisms and effector molecules contributing to JAK2 V617F-induced myeloproliferation and fibrosis. Here we show that JAK2 V617F promotes expression of oncostatin M (OSM) in neoplastic myeloid cells. Correspondingly, OSM was found to be overexpressed in the BM and elevated in the serum of patients with JAK2 V617F+ MPN. In addition, OSM secreted by JAK2 V617F+ cells stimulated growth of fibroblasts and microvascular endothelial cells and induced the production of angiogenic and profibrogenic cytokines (HGF, VEGF, and SDF-1) in BM fibroblasts. All effects of MPN cell-derived OSM were blocked by a neutralizing anti-OSM antibody, whereas the production of OSM in MPN cells was effectively suppressed by a pharmacologic JAK2 inhibitor or RNAi-mediated knockdown of JAK2. In summary, JAK2 V617F-mediated upregulation of OSM may contribute to fibrosis, neoangiogenesis, and the cytokine storm observed in JAK2 V617F+ MPN, suggesting that OSM could serve as a novel therapeutic target molecule in these neoplasms. IMR90 cells were treated with a single dose of rh Oncostatin M (10ng/ml).

2013-01-29 | E-GEOD-29655 | biostudies-arrayexpress

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