Component
Surface expression of endothelial leukocyte adhesion molecules
Surface expression of endothelial leukocyte adhesion molecules. Species, exposure and limitations are retained in each linked claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What acts on it
Sodium salicylate inhibited activation of nuclear factor kappa B by preventing phosphorylation and subsequent degradation of I-kappa-B-alpha without affecting tumour necrosis factor alpha-induced phosphorylation of ATF-2, blocked the increase in adhesion molecule messenger RNA and gave dose-dependent inhibition of surface vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 with higher doses required for endothelial-leukocyte adhesion molecule 1, and inhibited transendothelial migration of neutrophils; indomethacin, a nonsalicylate cyclooxygenase inhibitor, had no effect on surface expression, suggesting the effects were not due to inhibition of cyclooxygenase.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/aspirin-research/8621937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1", "start_char": 0, "end_char": 1767, "text_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1"}
- experimental_model
- Adhesion molecule expression, neutrophil adhesion and transendothelial migration in human umbilical vein endothelial cells
- exposure
- Sodium salicylate against tumour necrosis factor alpha stimulation, with indomethacin as a cyclooxygenase control
- limitations
- The indomethacin control is the important part: it shows the effect is not a cyclooxygenase effect. High salicylate concentrations, which the authors relate to high-dose therapy rather than to antiplatelet dosing.
- nutrient_topic
- Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. · Aspirin / acetylsalicylic acid
- organism
- Human cells
- plain_language
- A cyclooxygenase blocker does nothing here, so this arm of salicylate is not about prostaglandins at all.
- primary_references
- [asa-p8621937] Salicylates inhibit I kappa B-alpha phosphorylation, endothelial-leukocyte adhesion molecule expression, and neutrophil transmigration. (1996). https://pubmed.ncbi.nlm.nih.gov/8621937/ DOI: 10.4049/jimmunol.156.10.3961
- tissue_or_cell_type
- Endothelium
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adhesion molecule expression, neutrophil adhesion and transendothelial migration in human umbilical vein endothelial cells · source_derived_draft · unverified_draft
### asa-not-a-cyclooxygenase-effect Sodium salicylate inhibited activation of nuclear factor kappa B by preventing phosphorylation and subsequent degradation of I-kappa-B-alpha without affecting tumour necrosis factor alpha-induced phosphorylation of ATF-2, blocked the increase in adhesion molecule messenger RNA and gave dose-dependent inhibition of surface vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 with higher doses required for endothelial-leukocyte adhesion molecule 1, and inhibited transendothelial migration of neutrophils; indomethacin, a nonsalicylate cyclooxygenase inhibitor, had no effect on surface expression, suggesting the effects were not due to inhibition of cyclooxygenase. Condition category: normal nutrient_topic: Aspirin research collection; topical membership is not evidence of a direct clinical effect, and aspirin is recorded separately from salicylate, the metabolite it becomes. plain_language: A cyclooxygenase blocker does nothing here, so this arm of salicylate is not about prostaglandins at all. organism: Human cells tissue_or_cell_type: Endothelium experimental_model: Adhesion molecule expression, neutrophil adhesion and transendothelial migration in human umbilical vein endothelial cells limitations: The indomethacin control is the important part: it shows the effect is not a cyclooxygenase effect. High salicylate concentrations, which the authors relate to high-dose therapy rather than to antiplatelet dosing. exposure: Sodium salicylate against tumour necrosis factor alpha stimulation, with indomethacin as a cyclooxygenase control evidence_span: {"source_cache": "artifacts/aspirin-research/8621937.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1", "start_char": 0, "end_char": 1767, "text_sha256": "9b5aff676845bd0a47f25a0f63564880f70af7667b5ab9d667cece58d05356f1"} [asa-p8621937] Salicylates inhibit I kappa B-alpha phosphorylation, endothelial-leukocyte adhesion molecule expression, and neutrophil transmigration. (1996). https://pubmed.ncbi.nlm.nih.gov/8621937/ DOI: 10.4049/jimmunol.156.10.3961
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.