ArticleThe Biochemical journal1995
Enhanced complement susceptibility of avidin-biotin-treated human erythrocytes is a consequence of neutralization of the complement regulators CD59 and decay accelerating factor.
Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 45 citations in OpenAlex.
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- Red blood cell-derived materials for cancer therapy: Construction, distribution, and applications.Materials today. Bio · 2024Review
- Cyclic arginine-glycine-aspartic acid-modified red blood cells for drug delivery: Synthesis andJournal of pharmaceutical analysis · 2022Article
- Red blood cells: The metamorphosis of a neglected carrier into the natural mothership for artificial nanocarriers.Advanced drug delivery reviews · 2021Review
- Red Blood Cell Hitchhiking: A Novel Approach for Vascular Delivery of Nanocarriers.Annual review of biomedical engineering · 2021Article
- Cell-mediated and cell membrane-coated nanoparticles for drug delivery and cancer therapy.Cancer drug resistance (Alhambra, Calif.) · 2020Article
- Overexpression of CD59 inhibits apoptosis of T-acute lymphoblastic leukemia via AKT/Notch1 signaling pathway.Cancer cell international · 2019Article
- Red blood cells: Supercarriers for drugs, biologicals, and nanoparticles and inspiration for advanced delivery systems.Advanced drug delivery reviews · 2016Review
- Delivery of drugs bound to erythrocytes: new avenues for an old intravascular carrier.Therapeutic delivery · 2015Review
- Identification of a novel short peptide seal specific to CD59 and its effect on HeLa cell growth and apoptosis.Cellular oncology (Dordrecht, Netherlands) · 2012Article
- Drug delivery by red blood cells: vascular carriers designed by mother nature.Expert opinion on drug delivery · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Biotinylation of erythrocytes (E) followed by avidin cross-linking at specific sites has been suggested as a novel means of drug delivery. Upon avidin cross-linking, biotinylated E become complement-activating and highly susceptible to complement lysis, thus bringing about release of entrapped drug. We set out to examine the mechanisms of this biotin-avidin-induced lytic susceptibility, focusing on the effects of biotinylation and avidin cross-linking on the major E complement regulatory molecules, decay accelerating factor (DAF) and CD59. We demonstrate here that biotinylation of E, which does not render them complement activating, partially inhibits DAF but has little effect on CD59. Subsequent cross-linking with avidin causes complete inhibition of DAF and near complete loss of CD59 activity. Following cross-linking, DAF and CD59 become associated in high molecular mass avidin-containing complexes on the membrane. Incorporation of physiological amounts of CD59 into the membranes of biotinylated and avidin cross-linked E is sufficient to render these cells resistant to complement lysis whereas incorporation of DAF has relatively little effect. An understanding of the molecular mechanisms underlying complement susceptibility of biotin-avidin treated E should allow a rational design of strategies for drug delivery using E or other large, potentially complement-activating carriers.
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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.