Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Modur, Vijayanand; Feldhaus, Michael J.; Weyrich, Andrew S.; Jicha, Douglas L.; Prescott, Stephen M.; Zimmerman, Guy A.; McIntyre, Thomas M.

doi:10.1172/jci119508

Cited by 181 publications

(150 citation statements)

References 42 publications

(33 reference statements)

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“…Because endothelial cells have abundant OSM receptors, circulating OSM may play a role in initiating the inflammatory response by increasing adhesion molecule expression, PMN adhesion, and transmigration (Modur et al, 1997;Yao et al, 1996). In our patients, the normal plasma OSM levels and the OSM production by blood PMN ex vivo suggest that OSM is not involved in alveolar PMN recruitment.…”

Section: Grenier Et Almentioning

confidence: 61%

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Grenier

Combaux

Chastre

et al. 2001

Laboratory Investigation

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SUMMARY:Polymorphonuclear neutrophils (PMN) are involved in the pathogenesis of acute lung injury (ALI), secreting numerous mediators such as proteases, reactive oxygen species, and cytokines. Because we had recently observed the ability of normal human PMN to degranulate and synthesize oncostatin M (OSM), an IL-6 -family cytokine, we quantified OSM production ex vivo by highly purified blood and alveolar PMN from 24 ventilated patients with ALI, including some patients with severe pneumonia. Most of the patients had no detectable OSM in plasma, and OSM production by cultured blood PMN was similar to that of healthy controls. However, OSM was present in bronchoalveolar lavage (BAL) fluid supernatant, with significantly higher levels during pneumonia. In addition, alveolar OSM levels correlated with the number of PMN obtained by BAL, suggesting that PMN are an important source of OSM within the alveoli. Indeed, purified alveolar PMN from all of the patients, especially those with pneumonia, strongly produced OSM. Interestingly, in the latter patients, alveolar PMN always produced more OSM than autologous blood PMN. These results document the functional duality of PMN in ALI by showing the participation of PMN in the modulation of lung inflammation. (Lab Invest 2001, 81:133-141).

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Section: Grenier Et Almentioning

confidence: 61%

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Grenier

Combaux

Chastre

et al. 2001

Laboratory Investigation

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“…Existing evidence in the literature indicates that OSM mainly functions during tissue inflammation. Depending on the cellular context, OSM can exert either proinflammatory or antiinflammatory effects [64][65][66]. The facts that both OSM-null and OSMR-null mice are viable and appear to have no obvious developmental defects suggest that OSM and OSMR are less likely involved in normal embryonic myogenesis [67,68].…”

Section: The Role Of Osm In the Early Phase Of The Injury-induced Musmentioning

confidence: 99%

Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration

Xiao

Wang

et al. 2010

Cell Res

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Oncostatin M (OSM) is a cytokine of the interleukin-6 family and plays important roles during inflammation. However, its roles in myoblast differentiation and muscle regeneration remain unexplored. We show here that OSM potently inhibited myoblast differentiation mainly by activating the JAK1/STAT1/STAT3 pathway. OSM downregulated myocyte enhancer-binding factor 2A (MEF2A), upregulated the expression of Id1 and Id2, and inhibited the transcriptional activity of MyoD and MEF2. In addition, OSM also enhanced the expression of STAT3 and OSM receptor, which constituted a positive feedback loop to further amplify OSM-induced signaling. Moreover, we found that STAT1 physically associated with MEF2 and repressed its transcriptional activity, which could account for the OSM-mediated repression of MEF2. Although undetectable in normal muscles in vivo, OSM was rapidly induced on muscle injury and then promptly downregulated just before the majority of myoblasts differentiate. Prolonged expression of OSM in muscles compromised the regeneration process without affecting myoblast proliferation, suggesting that OSM functions to prevent proliferating myoblasts from premature differentiation during the early phase of muscle regeneration.

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“…For instance, an OSM-mediated increase in membrane-bound intercellular adhesion molecule may lead to higher recognition of tumor cells by cytotoxic lymphocytes. 37 On the other hand, OSM is involved in inflammation 40 and has implications in connective tissue disease. 36 Thus, although we were up to now not able to identify the molecular nature of AIF, the possibility of cytokine induction by integrated AAV with unwanted or unexpected effects may imply AAV pathogenicity and warrants careful consideration.…”

Section: Search For Cytokine Candidatesmentioning

confidence: 99%

Integration of adeno-associated virus 2 DNA in human MKR melanoma cells induces a peptide with oncosuppressive properties

Bantel-Schaal

2001

Int. J. Cancer

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Oncostatin M is a proinflammatory mediator. In vivo effects correlate with endothelial cell expression of inflammatory cytokines and adhesion molecules.

Cited by 181 publications

References 42 publications

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Oncostatin M Production by Blood and Alveolar Neutrophils during Acute Lung Injury

Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration

Integration of adeno-associated virus 2 DNA in human MKR melanoma cells induces a peptide with oncosuppressive properties

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