ArticleJournal of molecular medicine (Berlin, Germany)2011
Down-regulation of endothelial TLR4 signalling after apo A-I gene transfer contributes to improved survival in an experimental model of lipopolysaccharide-induced inflammation.
Article in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Association of high-density lipoprotein cholesterol lipid with peritoneal dialysis related peritonitis.BMC nephrology · 2026Article
- Inventive HDL Mimicking Nanoparticles: A Promising Frontier in Cardiovascular Disease Management.Cardiovascular toxicology · 2025Review
- Vitamin D immune modulation of the anti-inflammatory effects of HDL-associated proteins.Lipids in health and disease · 2025Review
- Association of cerebrospinal fluid NPY with peripheral ApoA: a moderation effect of BMI.Nutrition & metabolism · 2024Article
- Molecular Effect of Variants in Toll-like Receptor 4 Gene in Saudi Patients with Type 2 Diabetes Mellitus.Cells · 2023Article
- A Current Update on the Role of HDL-Based Nanomedicine in Targeting Macrophages in Cardiovascular Disease.Pharmaceutics · 2023Review
- Impact of High-Density Lipoproteins on Sepsis.International journal of molecular sciences · 2022Review
- High-Density Lipoproteins: A Role in Inflammation in COPD.International journal of molecular sciences · 2022Review
- Multifaced Roles of HDL in Sepsis and SARS-CoV-2 Infection: Renal Implications.International journal of molecular sciences · 2021Review
- Current Understanding of the Immunomodulatory Activities of High-Density Lipoproteins.Biomedicines · 2021Review
- Chymase released from hypoxia-activated cardiac mast cells cleaves human apoA-I at TyrJournal of lipid research · 2018Article
- Article
- Inflammation - Cause or Consequence of Heart Failure or Both?Current heart failure reports · 2017Review
- Heart Failure with Preserved Ejection Fraction and Future Pharmacological Strategies: a Glance in the Crystal Ball.Current cardiology reports · 2017Review
- Emerging Roles of Apolipoprotein E and Apolipoprotein A-I in the Pathogenesis and Treatment of Lung Disease.American journal of respiratory cell and molecular biology · 2016Review
- Carboxyl-Terminal Cleavage of Apolipoprotein A-I by Human Mast Cell Chymase Impairs Its Anti-Inflammatory Properties.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- High-density Lipoproteins and Apolipoprotein A-I: Potential New Players in the Prevention and Treatment of Lung Disease.Frontiers in pharmacology · 2016Review
- Apolipoprotein A-I gene transfer exerts immunomodulatory effects and reduces vascular inflammation and fibrosis in ob/ob mice.Journal of inflammation (London, England) · 2016Article
- The delta high-density lipoprotein cholesterol ratio: a novel parameter for gram-negative sepsis.SpringerPlus · 2016Article
- The Impact of Lipoproteins on Wound Healing: Topical HDL Therapy Corrects Delayed Wound Healing in Apolipoprotein E Deficient Mice.Pharmaceuticals (Basel, Switzerland) · 2014Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protective effects of high-density lipoprotein (HDL) under lipopolysaccharide (LPS) conditions have been well documented. Here, we investigated whether an effect of HDL on Toll-like receptor 4 (TLR4) expression and signalling may contribute to its endothelial-protective effects and to improved survival in a mouse model of LPS-induced inflammation and lethality. HDL cholesterol increased 1.7-fold (p<0.005) and lung endothelial TLR4 expression decreased 8.4-fold (p<0.005) 2 weeks after apolipoprotein (apo) A-I gene transfer. Following LPS administration in apo A-I gene transfer mice, lung TLR4 and lung MyD88 mRNA expression, reflecting TLR4 signalling, were 3.0-fold (p<0.05) and 2.1-fold (p<0.05) lower, respectively, than in LPS control mice. Concomitantly, LPS-induced lung neutrophil infiltration, lung oedema and mortality were significantly attenuated following apo A-I transfer. In vitro, supplementation of HDL or apo A-I to human microvascular endothelial cells-1 24 h before LPS administration reduced TLR4 expression, as assessed by fluorescent-activated cell sorting, and decreased the LPS-induced MyD88 mRNA expression and NF-κB activity, independently of LPS binding. In conclusion, HDL reduces TLR4 expression and signalling in endothelial cells, which may contribute significantly to the protective effects of HDL in LPS-induced inflammation and lethality.
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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.