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Exogenous Oncostatin M Induces Cardiac Dysfunction, Muscluloskeletal Atrophy and Fibrosis

ABSTRACT: Exogenous Oncostatin M Induces Cardiac Dysfunction, Muscluloskeletal Atrophy and Fibrosis

PROVIDER: PRJNA771673 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16355761_1.fastq.gz	Fastqsanger.gz
	SRR16355761_2.fastq.gz	Fastqsanger.gz
	SRR16355762_1.fastq.gz	Fastqsanger.gz
	SRR16355762_2.fastq.gz	Fastqsanger.gz
	SRR16355763_1.fastq.gz	Fastqsanger.gz

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Exogenous Oncostatin M Induces Cardiac Dysfunction, Muscluloskeletal Atrophy and Fibrosis

Project description:Musculoskeletal diseases such as muscular dystrophy, cachexia, osteoarthritis, and rheumatoid arthritis impair overall physical health. Patients suffer from increased pain and death rate, decreased productivity and function. Inflammation and fibrosis are commonly observed in musculoskeletal disorders either at the bone, muscle, or joint. The Interleukin-6 Family of Cytokines primarily Interleukin-6 (IL-6) are implicated in the context of musculoskeletal disorders. In this study, we utilized adeno-associated virus expressing murine Oncostatin M or an empty vector at 10^11 viral particles to observe effects in muscle and bone of mice in the presence and absence of Interleukin-6. We performed echocardiography, microCT, quantitative polymerase chain reaction, histology, and RNA-sequencing to characterize the functional effects on muscle and bone. The echocardiography results demonstrated cardiac dysfunction as shown by reduced ejection fraction (%) and fractional shortening (%) with AAV-Osm compared to AAV-Null. RNA-sequencing results on cardiac muscle showed increased cardiac inflammation and fibrosis genes with AAV-Osm. Skeletal muscle weights and histology revealed muscle atrophy and fibrosis in the gastrocnemius, tibialis anterior, and quadriceps of the local limbs injected with AAV-Osm, but not observed in the non-injected side. MicroCT results revealed local and distant trabecular bone loss with AAV-Osm as shown by reduced bone volume, number, thickness, and increased trabeculae separation. Our findings show that Oncostatin M induces cardiac dysfunction, muscle, and bone atrophy independent of Interleukin-6.

2022-10-04 | GSE185996 | GEO

Exogenous Oncostatin M induces Cardiac Dysfunction, Musculoskeletal Atrophy, and Fibrosis.

Project description:Musculoskeletal diseases such as muscular dystrophy, cachexia, osteoarthritis, and rheumatoid arthritis impair overall physical health and reduce survival. Patients suffer from pain, dysfunction, and dysmobility due to inflammation and fibrosis in bones, muscles, and joints, both locally and systemically. The Interleukin-6 (IL-6) family of cytokines, most notably IL-6, is implicated in musculoskeletal disorders and cachexia. Here we show elevated circulating levels of OSM in murine pancreatic cancer cachexia and evaluate the effects of the IL-6 family member, Oncostatin M (OSM), on muscle and bone using adeno-associated virus (AAV) mediated over-expression of murine OSM in wildtype and IL-6 deficient mice. Initial studies with high titer AAV-OSM injection yielded high circulating OSM and IL-6, thrombocytosis, inflammation, and 60% mortality without muscle loss within 4 days. Subsequently, to mimic OSM levels in cachexia, a lower titer of AAV-OSM was used in wildtype and Il6 null mice, observing effects out to 4 weeks and 12 weeks. AAV-OSM caused muscle atrophy and fibrosis in the gastrocnemius, tibialis anterior, and quadriceps of the injected limb, but these effects were not observed on the non-injected side. In contrast, OSM induced both local and distant trabecular bone loss as shown by reduced bone volume, trabecular number, and thickness, and increased trabecular separation. OSM caused cardiac dysfunction including reduced ejection fraction and reduced fractional shortening. RNA-sequencing of cardiac muscle revealed upregulation of genes related to inflammation and fibrosis. None of these effects were different in IL-6 knockout mice. Thus, OSM induces local muscle atrophy, systemic bone loss, tissue fibrosis, and cardiac dysfunction independently of IL-6, suggesting a role for OSM in musculoskeletal conditions with these characteristics, including cancer cachexia.

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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

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)]

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Macrophage hypoxia signaling regulates cardiac fibrosis via Oncostatin M.

Project description:The fibrogenic response in tissue-resident fibroblasts is determined by the balance between activation and repression signals from the tissue microenvironment. While the molecular pathways by which transforming growth factor-1 (TGF-β1) activates pro-fibrogenic mechanisms have been extensively studied and are recognized critical during fibrosis development, the factors regulating TGF-β1 signaling are poorly understood. Here we show that macrophage hypoxia signaling suppresses excessive fibrosis in a heart via oncostatin-m (OSM) secretion. During cardiac remodeling, Ly6Chi monocytes/macrophages accumulate in hypoxic areas through a hypoxia-inducible factor (HIF)-1α dependent manner and suppresses cardiac fibroblast activation. As an underlying molecular mechanism, we identify OSM, part of the interleukin 6 cytokine family, as a HIF-1α target gene, which directly inhibits the TGF-β1 mediated activation of cardiac fibroblasts through extracellular signal-regulated kinase 1/2-dependent phosphorylation of the SMAD linker region. These results demonstrate that macrophage hypoxia signaling regulates fibroblast activation through OSM secretion in vivo.

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Mechanism of Mitochondrial Dysfunction in Spinal and Bulbar Muscular Atrophy [RNA-seq]

Project description:Mechanism of Mitochondrial Dysfunction in Spinal and Bulbar Muscular Atrophy [RNA-seq]

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Mechanism of Mitochondrial Dysfunction in Spinal and Bulbar Muscular Atrophy [ChIP-seq]

Project description:Mechanism of Mitochondrial Dysfunction in Spinal and Bulbar Muscular Atrophy [ChIP-seq]

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