Trial reportThe Journal of biological chemistry2014
Proteolysis of apolipoprotein A-I by secretory phospholipase A₂: a new link between inflammation and atherosclerosis.
Trial report in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 32 citations in OpenAlex.
- Anti-Inflammatory HDL Function, Incident Cardiovascular Events, and Mortality: A Secondary Analysis of the JUPITER Randomized Clinical Trial.Journal of the American Heart Association · 2020 · on this mapTrial
- Group IIA Secretory Phospholipase AArteriosclerosis, thrombosis, and vascular biology · 2019Trial
- Metabolic challenges in rheumatoid arthritis: a translational overview from pathogenesis to patient care.Acta diabetologica · 2026Review
- Amyloidogenic 60-71 deletion/ValThr insertion mutation of apolipoprotein A-I generates a new aggregation-prone segment that promotes nucleation through entropic effects.Scientific reports · 2023Article
- Dyslipidemia in rheumatoid arthritis: the possible mechanisms.Frontiers in immunology · 2023Review
- Predictive Value of Perioperative Cytokine Levels on the Risk for In-Stent Restenosis in Acute Myocardial Infarction Patients.Contrast media & molecular imaging · 2022Article
- New insights into the emerging effects of inflammatory response on HDL particles structure and function.Molecular biology reports · 2021Review
- Pharmacological Characterisation ofInternational journal of molecular sciences · 2021Article
- The Relationship Between the Level of Serum ESM-1 and Lp-PLA2 in Patients With Acute ST-Segment Elevation Myocardial Infarction.Clinical and translational science · 2021Observational
- Adeno-Associated Virus VP1u Exhibits Protease Activity.Viruses · 2019Article
- Article
- Triglyceride increase in the core of high-density lipoproteins augments apolipoprotein dissociation from the surface: Potential implications for treatment of apolipoprotein deposition diseases.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- MicroRNA-1907 enhances atherosclerosis-associated endothelial cell apoptosis by suppressing Bcl-2.American journal of translational research · 2017Article
- Increased expression of ApoA1 after neuronal injury may be beneficial for healing.Molecular and cellular biochemistry · 2017Article
- MiR-129-5p-mediated Beclin-1 suppression inhibits endothelial cell autophagy in atherosclerosis.American journal of translational research · 2016Article
- Macrophage autophagy regulated by miR-384-5p-mediated control of Beclin-1 plays a role in the development of atherosclerosis.American journal of translational research · 2016Article
- Structural stability and functional remodeling of high-density lipoproteins.FEBS letters · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In the acute phase of the inflammatory response, secretory phospholipase A2 (sPLA2) reaches its maximum levels in plasma, where it is mostly associated with high density lipoproteins (HDL). Overexpression of human sPLA2 in transgenic mice reduces both HDL cholesterol and apolipoprotein A-I (apoA-I) plasma levels through increased HDL catabolism by an unknown mechanism. To identify unknown PLA2-mediated activities on the molecular components of HDL, we characterized the protein and lipid products of the PLA2 reaction with HDL. Consistent with previous studies, hydrolysis of HDL phospholipids by PLA2 reduced the particle size without changing its protein composition. However, when HDL was destabilized in the presence of PLA2 by the action of cholesteryl ester transfer protein or by guanidine hydrochloride treatment, a fraction of apoA-I, but no other proteins, dissociated from the particle and was rapidly cleaved. Incubation of PLA2 with lipid-free apoA-I produced similar protein fragments in the range of 6-15 kDa, suggesting specific and direct reaction of PLA2 with apoA-I. Mass spectrometry analysis of isolated proteolytic fragments indicated at least two major cleavage sites at the C-terminal and the central domain of apoA-I. ApoA-I proteolysis by PLA2 was Ca(2+)-independent, implicating a different mechanism from the Ca(2+)-dependent PLA2-mediated phospholipid hydrolysis. Inhibition of proteolysis by benzamidine suggests that the proteolytic and lipolytic activities of PLA2 proceed through different mechanisms. Our study identifies a previously unknown proteolytic activity of PLA2 that is specific to apoA-I and may contribute to the enhanced catabolism of apoA-I in inflammation and atherosclerosis.
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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.