ArticleThe Journal of experimental medicine1996
Interleukin 4 or oncostatin M induces a prolonged increase in P-selectin mRNA and protein in human endothelial cells.
Article in The Journal of experimental medicine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 242 citations in OpenAlex.
- Soluble platelet selectin (sP-selectin) and soluble vascular cell adhesion molecule-1 (sVCAM-1) decrease during therapy with benznidazole in children with indeterminate form of Chagas' disease.Clinical and experimental immunology · 1999Trial
- NIR-II scattering gold superclusters for intravascular optical coherence tomography molecular imaging.Nature nanotechnology · 2025Article
- Single and consecutive 10-day remote ischemic preconditioning modify physical performance, post-exercise exerkine levels, and inflammation.Frontiers in physiology · 2024Article
- Prediction of Potential Biomarkers in Early-Stage Nasopharyngeal Carcinoma Based on Platelet RNA Sequencing.Molecular biotechnology · 2023Article
- Multi-organ single-cell analysis reveals an on/off switch system with potential for personalized treatment of immunological diseases.Cell reports. Medicine · 2023Article
- Review
- miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach.BMC research notes · 2022Article
- Tissue Proteomic Analysis Identifies Mechanisms and Stages of Immunopathology in Fatal COVID-19.American journal of respiratory cell and molecular biology · 2022Article
- Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection.Scientific reports · 2021Article
- Sickle cell vaso-occlusion: The dialectic between red cells and white cells.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- The role of the oncostatin M/OSM receptor β axis in activating dermal microvascular endothelial cells in systemic sclerosis.Arthritis research & therapy · 2020Article
- Article
- Human endothelial cells size-select their secretory granules for exocytosis to modulate their functional output.Journal of thrombosis and haemostasis : JTH · 2020Article
- Active roles of dysfunctional vascular endothelium in fibrosis and cancer.Journal of biomedical science · 2019Review
- Endothelial signaling by neutrophil-released oncostatin M enhances P-selectin-dependent inflammation and thrombosis.Blood advances · 2019Article
- Impaired frequencies and function of platelets and tissue remodeling in chronic Chagas disease.PloS one · 2019Article
- Coordination of Immune-Stroma Crosstalk by IL-6 Family Cytokines.Frontiers in immunology · 2019Review
- STAT3 Mediates the Differential Effects of Oncostatin M and TNFα on RA Synovial Fibroblast and Endothelial Cell Function.Frontiers in immunology · 2019Article
- Oncostatin M and its role in fibrosis.Connective tissue research · 2019Review
- Genome-Wide Transcriptional and Functional Analysis of Human T Lymphocytes Treated with Benzo[International journal of molecular sciences · 2018Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
During acute inflammation, P-selectin is transiently mobilized from Weibel-Palade bodies to the surface of histamine-activated endothelial cells, where it mediates rolling adhesion of neutrophils under hydrodynamic flow. During chronic or allergic inflammation, sustained expression of P-selectin on the endothelial cell surface has been observed. We found that the cytokines interleukin 4 (IL-4) or oncostatin M (OSM) induced a five- to ninefold increase in P-selectin messenger RNA (mRNA) in human umbilical vein endothelial cells (HUVEC) that persisted as long as 72 h. IL-4 elevated P-selectin mRNA by increasing its transcription rate rather than by prolonging its already long half-life. Stimulation of P-selectin transcription by IL-4 or OSM required new protein synthesis and tyrosine phosphorylation of cellular proteins. Tumor necrosis factor alpha, IL-1 beta, lipopolysaccharide, or IL-3 did not increase P-selectin mRNA in HUVEC, and did not augment the IL-4-induced increase in P-selectin transcripts. IL-4 or OSM increased P-selectin protein on the cell surface as well as in Weibel-Palade bodies. Under flow conditions, neutrophils rolled on P-selectin expressed by IL-4-treated HUVEC, and even more neutrophils rolled on P-selectin after IL-4-treated HUVEC were stimulated with histamine. These data demonstrate that IL-4 or OSM stimulates endothelial cells to synthesize more P-selectin over prolonged periods. The increased expression of P-selectin may facilitate the emigration of leukocytes into sites of chronic or allergic inflammation.
Indexed as
Identifiers
What OpenQuestion holds
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.