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Cited by 87Complement system in diseasesCell Adhesion Molecules ResearchNitric Oxide and Endothelin Effects

The DOI matches its Crossref record, with a small difference in title or year; 32 of the 32 references it cites were found in a registry or an index.

Endothelial Cell Activation by Pore-Forming Structures: Pivotal Role for Interleukin-1α

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Saadi, Soheyla, Holzknecht, Robert A., Patte, Christian P., Platt, Jeffrey L.·2000·Circulation
DOI 10.1161/01.cir.101.15.1867
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Abstract

Background —Interaction of complement with endothelial cells (ECs) underlies the development of inflammation and coagulation in disease. Assembly of the membrane attack complex (MAC) of complement on EC membrane, like stimulation with cytokines, upregulates tissue factor and cyclooxygenase-2 but does so via the intermediary action of IL-1α. We asked whether the MAC activates porcine aortic and microvascular ECs in a global manner by this mechanism and whether this mechanism is used by membrane pore-forming structures. Methods and Results —Exposure of ECs to complement caused upregulation of mRNAs for E-selectin, intracellular adhesion molecule-1, vascular cell adhesion molecule-1, Iκ-Bα, interleukin (IL)-1α, IL-1β, IL-8, and plasminogen activator inhibitor-1 over a period of 6 hours. The expression of these genes was not a primary response to stimulation, however, because IL-1 receptor antagonist inhibited expression of these genes. Activation of ECs by complement depended on the autocrine action of IL-1α, because complement-mediated EC activation was inhibited by anti–IL-1α antibodies. Melittin and mastoparan, amphiphilic pore-forming peptides like the MAC, induced E-selectin through intermediary action of IL-1. Conclusions —These findings suggest that transmembrane pore-forming proteins, as a class of molecules, activate ECs through the autocrine effects of IL-1α.

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Research works printed but not linked: 1

  1. Nishida M, Carley WW, Gerritsen ME, Ellingsen O, Kelly RA, Smith TW. Isolation and characterization of human and rat cardiac microvascular EC. Am J Physiol. 1993;264:H639–H652.

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Metadata

Authors
Saadi, S., Holzknecht, R. A., Patte, C. P., & Platt, J. L.
Affiliations
Mayo Clinic (US)
ORCID
Platt, Jeffrey L.
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2000-04-18
Volume
101
Issue
15
Pages
1867-1873
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.101.15.1867
OpenAlex
W2013535285
Cited by
87
References
32
Citations by year
2024: 1 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 1 · 2015: 3 · 2014: 2 · 2012: 5
FWCI
2.59
Type
journal article
Language
en
Open access
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (HL-46810, HL52297, R01HL046810)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords
endothelial activation, complement system, membrane attack complex, pore-forming peptides, melittin, mastoparan, interleukin-1 alpha, autocrine signaling, E-selectin, adhesion molecules, interleukin-1 receptor antagonist, inflammation, coagulation, microvascular endothelium
MeSH terms
Animals, Complement Activation, Endothelium, Vascular, Interleukin-1, Kinetics, Membrane Proteins, RNA, Messenger, Swine, Up-Regulation, Complement Membrane Attack Complex, E-Selectin

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