Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA325836 | ENA |
REPOSITORIES: ENA
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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
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
Project description:Cachexia is an exacerbating event in many types of cancer that is strongly associated with a poor prognosis. We have identified cytokine, signaling and transcription factors that are required for cachexia in the mouse C26 colon carcinoma model of cancer. C2C12 myotubes treated with conditioned medium from C26 cancer cells induced atrophy and activated a STAT-dependent reporter gene but not reporter genes dependent on SMAD, FOXO, C/EBP, NF-ĸB, or AP-1. Of the gp130 family members IL-11, IL-6, oncostatin M (OSM), and leukemia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the STAT reporter in myotubes. A LIF blocking antibody abolished C26 CM-induced STAT reporter activation STAT3 phosphorylation and myotube atrophy, but blocking antibodies to IL-6 or OSM did not. JAK2 inhibitors also blocked the C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atrophy in myotubes. LIF at levels found in the C26 CM was sufficient for STAT reporter activation and atrophy in myotubes. In vivo, an increase in serum LIF preceded the increase in IL-6 in mice with C26 tumors. Overexpression of a dominant negative Stat3Cβ-EGFP gene in myotubes and in mouse muscle blocked the atrophy caused by C26 CM or C26 tumors, respectively. Taken together these data support an important role of LIF- JAK2-STAT3 in C26 cachexia and point to a therapeutic approach for at least some types of cancer cachexia. from three replicate wells of cells at each treatment, pools of total RNA were used to create cDNA which were evaluated on Affymetrix mouse gene 1.0 ST v.1 arrays.
2015-06-25 | E-GEOD-68827 | biostudies-arrayexpress
Project description:Cachexia is an exacerbating event in many types of cancer that is strongly associated with a poor prognosis. We have identified cytokine, signaling and transcription factors that are required for cachexia in the mouse C26 colon carcinoma model of cancer. C2C12 myotubes treated with conditioned medium from C26 cancer cells induced atrophy and activated a STAT-dependent reporter gene but not reporter genes dependent on SMAD, FOXO, C/EBP, NF-ĸB, or AP-1. Of the gp130 family members IL-11, IL-6, oncostatin M (OSM), and leukemia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the STAT reporter in myotubes. A LIF blocking antibody abolished C26 CM-induced STAT reporter activation STAT3 phosphorylation and myotube atrophy, but blocking antibodies to IL-6 or OSM did not. JAK2 inhibitors also blocked the C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atrophy in myotubes. LIF at levels found in the C26 CM was sufficient for STAT reporter activation and atrophy in myotubes. In vivo, an increase in serum LIF preceded the increase in IL-6 in mice with C26 tumors. Overexpression of a dominant negative Stat3Cβ-EGFP gene in myotubes and in mouse muscle blocked the atrophy caused by C26 CM or C26 tumors, respectively. Taken together these data support an important role of LIF- JAK2-STAT3 in C26 cachexia and point to a therapeutic approach for at least some types of cancer cachexia.
2015-06-25 | GSE68827 | GEO
Project description:It has been well established that (LIF) is essential for maintaining naive pluripotency of ESCs. Oncostatin M (OSM) is a member of the IL-6 family of cytokines which share gp130 as a receptor subunit, and the OSM-gp130 complex can recruit either LIF receptor β or OSM receptor β. Here we show that OSM can completely replace LIF to maintain naive pluripotency of mouse ESCs. Mouse ESCs cultured in the presence of LIF or OSM not only express pluripotency genes at similar levels but also exhibit the same developmental pluripotency as evidenced by generation of germline competent chimeras, supporting previous findings. Moreover, we demonstrate that mESCs cultured in OSM produce viable all-ESC pups by tetraploid embryo complementation (TEC) assay, the most stringent functional test of authentic pluripotency. Furthermore, the telomere length and telomerase activity also are crucial for unlimited self-renewal and genomic stability of mESCs, and these do not differ in mESCs cultured under OSM or LIF. The transcriptome of mESCs cultured in OSM overall is very similar to that of LIF, and OSM activates Stat3 signaling pathway, like LIF. Additionally, OSM upregulates pentose and glucuronate interconversions, ascorbate and aldarate metabolism, steroid and retinol metabolism pathways. Although the significance of these pathways remains to be determined, our data shows that OSM can maintain the naive pluripotent stem cells in the absence of LIF.
2021-01-23 | GSE165292 | GEO
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
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
Project description:Examination of transcriptional responses to Embryonic stem cell differentiation in the Brca1 (+/+) cell line AB2.2 compared to Brca1 (+/-) cell line PL2F8 Total RNA obtained from murine Stem cell lines AB2.2 and PL2F8 at 0,2,4,6,8 days following induction of differentiation via the removal of the Leukemia Inhibitory factor (LIF).
2012-12-31 | E-GEOD-24248 | biostudies-arrayexpress
Project description:Proper regulation of the proliferation and differentiation of radial glia (RG), the neural stem cells of the developing cortex, is fundamental for brain growth and organization. In humans, a specialized RG subtype, the outer radial glia (oRG), are abundant and give rise to diverse neuronal and glial progeny. However, the mechanisms regulating oRG development and differentiation are not fully understood. Here we investigated the regulation of oRG expansion and lineage potential by perturbing Leukemia Inhibitory Factor (LIF) signaling in the developing human cortex and in human pluripotent stem cell (PSC)-derived cortical organoids. LIF receptors are specifically expressed in oRG cells during neurogenesis, and, consistent with the previously described role of this cytokine as an activator of stem cell self-renewal, LIF treatment increased the number of oRG cells. Surprisingly, LIF treatment also increased the production of inhibitory interneurons (INs) in the cortex. Comparative transcriptomic analysis suggested that these INs resemble INs produced in the caudal ganglionic eminence (CGE). To test if oRG cells are the progenitors of these CGE-like INs, we isolated oRG cells from primary developing cortex and cultured them for several weeks with and without LIF treatment. We found that CGE-like INs were produced by oRG cells, and their abundance is increased by LIF treatment. Together, these observations suggest that LIF signaling regulates oRG lineage potential and capacity to generate CGE-like INs.
2023-03-23 | GSE227640 | GEO
Project description:pDCs selectively express the receptor for leukemia inhibitory factor (LIF) that signals through STAT3. We performed microarray analysis of primary pDCs sorted from bone marrow of C57BL6 mice and incubated with a) medium; b) LIF; c) CpG; d) LIF plus CpG.
2020-02-18 | GSE138018 | GEO