ArticleThe American journal of pathology1996
The membrane attack complex of complement induces interleukin-8 and monocyte chemoattractant protein-1 secretion from human umbilical vein endothelial cells.
Article in The American journal of pathology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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Who cites it
44 citing papers in PubMed, 160 citations in OpenAlex.
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- Single-Cell Transcriptomics Reveals Evidence of Endothelial Dysfunction in the Brains of COVID-19 Patients with Implications for Glioblastoma Progression.Brain sciences · 2023Article
- Increased plasma level of terminal complement complex in AMD patients: potential functional consequences for RPE cells.Frontiers in immunology · 2023Article
- Brain edema formation and therapy after intracerebral hemorrhage.Neurobiology of disease · 2023Review
- Exploratory Investigation of the Plasma Proteome Associated with the Endotheliopathy of Trauma.International journal of molecular sciences · 2022Article
- The Immunological Role of Vascular and Lymphatic Endothelial Cells in Filarial Infections.Animals : an open access journal from MDPI · 2022Review
- Nonsynonymous amino acid changes in the α-chain of complement component 5 influence longitudinal susceptibility toFrontiers in genetics · 2022Article
- Complement as driver of systemic inflammation and organ failure in trauma, burn, and sepsis.Seminars in immunopathology · 2021Review
- Platelet-Derived Growth Factor-D Activates Complement System to Propagate Macrophage Polarization and Neovascularization.Frontiers in cell and developmental biology · 2021Article
- Membrane Attack Complex in Myocardial Ischemia/Reperfusion Injury: A Systematic Review for Post Mortem Applications.Diagnostics (Basel, Switzerland) · 2020Review
- Progenitor-derived human endothelial cells evade alloimmunity by CRISPR/Cas9-mediated complete ablation of MHC expression.JCI insight · 2019Article
- Significance of Complement System in Ischemic Stroke: A Comprehensive Review.Aging and disease · 2019Review
- Bioactive Sphingolipids, Complement Cascade, and Free Hemoglobin Levels in Stable Coronary Artery Disease and Acute Myocardial Infarction.Mediators of inflammation · 2018Article
- Alloantibody and complement promote T cell-mediated cardiac allograft vasculopathy through noncanonical nuclear factor-κB signaling in endothelial cells.Circulation · 2013Article
- Article
- Selective inhibition of the master regulator transcription factor Egr-1 with catalytic oligonucleotides reduces myocardial injury and improves left ventricular systolic function in a preclinical model of myocardial infarction.Journal of the American Heart Association · 2013Article
- Complement activation and cardiac surgery: a novel target for improving outcomes.Anesthesia and analgesia · 2012Review
- Live Brugia malayi microfilariae inhibit transendothelial migration of neutrophils and monocytes.PLoS neglected tropical diseases · 2012Article
- Sub-lytic C5b-9 induces functional changes in retinal pigment epithelial cells consistent with age-related macular degeneration.Eye (London, England) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell surface assembly of the membrane attack complex (MAC) of complement occurs in a variety of pathophysiological settings. Depending upon the density and size distribution of pores formed by the MAC and the functional integrity of membrane regulators of complement activation, the MAC can either cause direct cell lysis or transduce cell activation. We have examined the functional capacity of sublytic concentrations of MAC to induce the secretion of specific alpha- and beta-chemokines from human umbilical vein endothelial cells (HUVECs). Endothelial cell activation by the MAC has particular relevance to complement-dependent inflammatory processes including ischemia-reperfusion injury and acute lung injury. Assembly of sublytic concentrations of the MAC on HUVECs resulted in the sequential secretion of both neutrophil and monocyte chemotactic activities. Analysis of conditioned medium from MAC-bearing HUVECs revealed that the neutrophil chemotactic activity was largely attributable to interleukin (IL)-8, whereas the monocyte chemotactic activity, which was detected later (peak at 8 hours versus 4 hours), was largely attributable to MCP-1. This temporal pattern of MAC-induced secretion of IL-8 and MCP-1 was confirmed using IL-8- and MCP-1-specific enzyme-linked immunosorbent assays. Northern hybridization analysis of HUVECs revealed that MAC deposition was accompanied by an increase in IL-8 and MCP-1 mRNA levels. These data indicate that assembly of sublytic concentrations of the MAC on HUVECs can induce the sequential secretion of both neutrophil and monocyte chemotactic activities and that the former is largely attributable to IL-8 whereas the latter is largely attributable to MCP-1.
Indexed as
Identifiers
8780399PMC1865152W1961339089What 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.