ArticleExperimental biology and medicine (Maywood, N.J.)2021
Proteinase 3 contributes to endothelial dysfunction in an experimental model of sepsis.
Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Choline supplementation protects against sepsis-induced lung injury, potentially through suppression of Prtn3-associated monocyte activation.Frontiers in pharmacology · 2026Article
- Proteinase 3 is involved in presepsin production through neutrophil extracellular trap phagocytosis by macrophages.Scientific reports · 2025Article
- Versatile roles for neutrophil proteinase 3 in hematopoiesis and inflammation.Immunologic research · 2024Review
- Molecular profiling of frontal and occipital subcortical white matter hyperintensities in Alzheimer's disease.bioRxiv : the preprint server for biology · 2024Article
- Molecular profiling of frontal and occipital subcortical white matter hyperintensities in Alzheimer's disease.Frontiers in neurology · 2024Article
- Morfofunctional and Molecular Changes in Placenta and Peripheral Blood in Preeclampsia and Gestational Diabetes Mellitus.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2023Article
- Novel plasma protein biomarkers from critically ill sepsis patients.Clinical proteomics · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In sepsis-induced inflammation, polymorphonuclear neutrophils (PMNs) contribute to vascular dysfunction. The serine proteases proteinase 3 (PR3) and human leukocyte elastase (HLE) are abundant in PMNs and are released upon degranulation. While HLE's role in inflammation-induced endothelial dysfunction is well studied, PR3's role is largely uninvestigated. We hypothesized that PR3, similarly to HLE, contributes to vascular barrier dysfunction in sepsis. Plasma PR3 and HLE concentrations and their leukocyte mRNA levels were measured by ELISA and qPCR, respectively, in sepsis patients and controls. Exogenous PR3 or HLE was applied to human umbilical vein endothelial cells (HUVECs) and HUVEC dysfunction was assessed by FITC-dextran permeability and electrical resistance. Both PR3 and HLE protein and mRNA levels were significantly increased in sepsis patients (
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