ArticleMolecular biology reports2015
Differential pro-inflammatory responses of TNF-α receptors (TNFR1 and TNFR2) on LOX-1 signalling.
Article in Molecular biology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Factors influencing glycocalyx degradation: a narrative review.Frontiers in immunology · 2024Review
- The genesis of cardiovascular risk in inflammatory arthritis: insights into glycocalyx shedding, endothelial dysfunction, and atherosclerosis initiation.Clinical rheumatology · 2023Review
- High Plasma Levels of Soluble Lectin-like Oxidized Low-Density Lipoprotein Receptor-1 Are Associated With Inflammation and Cardiometabolic Risk Profiles in Pediatric Overweight and Obesity.Journal of the American Heart Association · 2023Article
- Metabolic Syndrome and Psoriasis: Mechanisms and Future Directions.Frontiers in immunology · 2021Review
- Inflammation and tissue homeostasis: the NF-κB system in physiology and malignant progression.Molecular biology reports · 2020Review
- Interleukin-1β Promotes Ox-LDL Uptake by Human Glomerular Mesangial Cells via LOX-1.International journal of medical sciences · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF-α potently induces LOX-1 expression in THP-1 macrophages at concentrations between 1.25-50 ng/mL. The interplay between the two TNF receptors (TNFR1 and TNFR2) was apparent in the expression pattern of LOX-1 in response to TNF-α. Interestingly, R1 signal abrogation depleted both TNFR2 as well as LOX-1 transcript expression, suggesting that TNFR1 holds priority in the relative signaling mechanism between TNFR1 and TNFR2. TNF-α was also found to abrogate the oxidized-LDL (ox-LDL) mediated increase in intracellular pool of NO, a known downstream intermediate of LOX-1 pro-inflammatory signaling cascade. At the level of ox-LDL clearance, TNF-α inhibited the uptake (scavenging) of ox-LDL via LOX-1. Our study demonstrates the ability of TNF-α to enhance the signaling propensity of LOX-1 by increasing its expression and inhibiting its scavenging property.
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