ArticleAmerican journal of physiology. Cell physiology2011
Endothelium-derived GM-CSF influences expression of oncostatin M.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Skin-derived G-CSF activates pathological granulopoiesis upon psoriasis.EMBO molecular medicine · 2026Article
- Stigmasterol Decreases Oncostatin M Production Through Suppressing PI3K/Akt/NF-κB Signaling Processes in Neutrophil-like Differentiated HL-60 Cells.Biomedicines · 2026Article
- Naringenin, a Food Bioactive Compound, Reduces Oncostatin M Through Blockade of PI3K/Akt/NF-κB Signal Pathway in Neutrophil-like Differentiated HL-60 Cells.Foods (Basel, Switzerland) · 2025Article
- Tryptanthrin Down-Regulates Oncostatin M by Targeting GM-CSF-Mediated PI3K-AKT-NF-κB Axis.Nutrients · 2024Article
- Target Role of Monocytes as Key Cells of Innate Immunity in Rheumatoid Arthritis.Diseases (Basel, Switzerland) · 2024Review
- Oncostatin M: Dual Regulator of the Skeletal and Hematopoietic Systems.Current osteoporosis reports · 2024Review
- Hydrogen Sulfide Downregulates Oncostatin M Expression via PI3K/Akt/NF-κB Signaling Processes in Neutrophil-like Differentiated HL-60 Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Oncostatin M regulates hematopoietic stem cell (HSC) niches in the bone marrow to restrict HSC mobilization.Leukemia · 2022Article
- Resveratrol Downregulates Granulocyte-Macrophage Colony-Stimulating Factor-Induced Oncostatin M Production through Blocking of PI3K/Akt/NF-κB Signal Cascade in Neutrophil-like Differentiated HL-60 Cells.Current issues in molecular biology · 2022Article
- Polymorphonuclear Neutrophils and Tumors: Friend or Foe?Experientia supplementum (2012) · 2022Article
- Dexamethasone Attenuates Oncostatin M Production via Suppressing of PI3K/Akt/NF-κB Signaling in Neutrophil-like Differentiated HL-60 Cells.Molecules (Basel, Switzerland) · 2021Article
- Endothelial signaling by neutrophil-released oncostatin M enhances P-selectin-dependent inflammation and thrombosis.Blood advances · 2019Article
- The barrier hypothesis and Oncostatin M: Restoration of epithelial barrier function as a novel therapeutic strategy for the treatment of type 2 inflammatory disease.Tissue barriers · 2017Review
- Neutrophils are a major source of the epithelial barrier disrupting cytokine oncostatin M in patients with mucosal airways disease.The Journal of allergy and clinical immunology · 2017Article
- Intracerebral GM-CSF contributes to transendothelial monocyte migration in APP/PS1 Alzheimer's disease mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
During and after transendothelial migration, neutrophils undergo a number of phenotypic changes resulting from encounters with endothelium-derived factors. This report uses an in vitro model with human umbilical vein endothelial cells and isolated human neutrophils to examine the effects of two locally derived cytokines, granulocyte (G)-macrophage (M) colony-stimulating factor (GM-CSF) and G-CSF, on oncostatin M (OSM) expression. Neutrophils contacting activated HUVEC expressed and released increased amounts of oncostatin M (OSM), a proinflammatory cytokine known to induce polymorphonuclear neutrophil adhesion and chemotaxis. Neutrophil transendothelial migration resulted in threefold higher OSM expression and protein levels compared with nontransmigrated cells. Addition of anti-GM-CSF neutralizing antibody reduced OSM expression level but anti-G-CSF was without effect. GM-CSF but not G-CSF protein addition to cultures of isolated neutrophils resulted in a significant increase in OSM protein secretion. However, inhibition of β(2) integrins by neutralizing antibody significantly reduced GM-CSF-induced OSM production indicating this phenomenon is adhesion dependent. Thus cytokine-stimulated endothelial cells can produce sufficient quantities of GM-CSF to influence in an adhesion-dependent manner, the phenotypic characteristics of neutrophils resulting in the latter's transmigration. Both transmigration and adhesion phenomenon lead to increased production of OSM by neutrophils that then play a major role in inflammatory response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.