ArticleThe American journal of pathology1993
Regulation of complement membrane attack complex formation in myocardial infarction.
Article in The American journal of pathology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 83 citations in OpenAlex.
- Behavior of Complement System Effectors in Chronic and Acute Coronary Artery Disease.Journal of clinical medicine · 2025Article
- Shedding of membrane complement inhibitors CD59 and CD46 into the circulation is associated with poor prognosis in acute coronary syndrome patients: a cohort study.Journal of translational medicine · 2024Article
- The Alternative Complement Pathway Is Activated Without a Corresponding Terminal Pathway Activation in Patients With Heart Failure.Frontiers in immunology · 2021Article
- Membrane Attack Complex in Myocardial Ischemia/Reperfusion Injury: A Systematic Review for Post Mortem Applications.Diagnostics (Basel, Switzerland) · 2020Review
- Complement Activation in Association with Markers of Neutrophil Extracellular Traps and Acute Myocardial Infarction in Stable Coronary Artery Disease.Mediators of inflammation · 2020Article
- Article
- Targeting of exon VI-skipping human RGR-opsin to the plasma membrane of pigment epithelium and co-localization with terminal complement complex C5b-9.Molecular vision · 2016Article
- Validation of the vitronectin knockout mouse as a model for studying myocardial infarction: Vitronectin appears to influence left ventricular remodelling following myocardial infarction.Experimental and clinical cardiology · 2013Article
- Identification of a novel short peptide seal specific to CD59 and its effect on HeLa cell growth and apoptosis.Cellular oncology (Dordrecht, Netherlands) · 2012Article
- Dynamic control of the complement system by modulated expression of regulatory proteins.Laboratory investigation; a journal of technical methods and pathology · 2011Review
- Complement regulator CD59 protects against atherosclerosis by restricting the formation of complement membrane attack complex.Circulation research · 2009Article
- Human natural IgM can induce ischemia/reperfusion injury in a murine intestinal model.Molecular immunology · 2008Article
- Inhibition of classical complement activation attenuates liver ischaemia and reperfusion injury in a rat model.Clinical and experimental immunology · 2006Article
- Complement activation and expression of membrane regulators in the middle ear mucosa in otitis media with effusion.Clinical and experimental immunology · 1999Article
- Membrane attack complex of complement and 20 kDa homologous restriction factor (CD59) in myocardial infarction.Virchows Archiv : an international journal of pathology · 1997Article
- Complement in acute and chronic arthritides: assessment of C3c, C9, and protectin (CD59) in synovial membrane.Annals of the rheumatic diseases · 1996Article
- The membrane attack complex of complement induces interleukin-8 and monocyte chemoattractant protein-1 secretion from human umbilical vein endothelial cells.The American journal of pathology · 1996Article
- Time course of complement activation and inhibitor expression after ischemic injury of rat myocardium.The American journal of pathology · 1994Article
- Co-deposition of clusterin with the complement membrane attack complex in myocardial infarction.Immunology · 1993Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have suggested that the complement (C) system is involved in the development of tissue injury of myocardial infarction. As it is not known why the strictly controlled C system starts to react against autologous heart tissue, we have analyzed the expression of various membrane regulators of C (CR1, DAF, MCP, CD59, C8 binding protein) and the pattern of deposition of C components and plasma C regulators (C4b binding protein and vitronectin) in normal (n = 7) and infarcted (n = 13) human myocardium. In the infarcted myocardium deposits of the C membrane attack complex (MAC) were observed by immunofluorescence microscopy, and lesions resembling the transmembrane channels of MAC were detected by transmission electron microscopy. CD59 and C8 binding protein were strongly expressed by muscle cells of normal myocardial tissue. Little or no CR1, MCP, and DAF was observed on these cells. The assembly of MAC was accompanied by the deposition of vitronectin (S-protein) and C4b binding protein in the infarcted areas of myocardium. In accordance with our earlier results the expression of CD59 but not of C8 binding protein was clearly diminished in the lesions. The results show that C8 binding protein, vitronectin, and C4b binding protein do not prevent complement attack against the infarcted myocardium but rather become codeposited with the MAC. Ischemia-induced transformation of nonviable cells into complement activators, acquired loss of resistance to the MAC by shedding of CD59, and recruitment of multifunctional serum proteins by MAC could thus constitute a general process aimed at the clearance of injured tissue.
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Identifiers
7686345PMC1886952W168399381What 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.