Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Protection against complement-mediated cell damage by Ca2+ and Zn2+.

K J Micklem1, G M Alder, C D Buckley

  • 1Nuffield Department of Pathology, John Radcliffe Hospital, Oxford, UK.

Complement (Basel, Switzerland)
|January 1, 1988
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

11β-HSD1 plays a critical role in trabecular bone loss associated with systemic glucocorticoid therapy.

Arthritis research & therapy·2019
Same author

11 Beta-hydroxysteroid dehydrogenase type 1 regulates synovitis, joint destruction, and systemic bone loss in chronic polyarthritis.

Journal of autoimmunity·2018
Same author

Stroma: the forgotten cells of innate immune memory.

Clinical and experimental immunology·2018
Same author

Multimerin-2 is a ligand for group 14 family C-type lectins CLEC14A, CD93 and CD248 spanning the endothelial pericyte interface.

Oncogene·2017
Same author

The role of stromal cells in inflammatory bone loss.

Clinical and experimental immunology·2017
Same author

Treatment of inflammatory arthritis via targeting of tristetraprolin, a master regulator of pro-inflammatory gene expression.

Annals of the rheumatic diseases·2016
Same journal

Patients with CLL and hypocomplementaemia have an impaired serum bactericidal activity against the Salmonella minnesota Re mutant.

Complement (Basel, Switzerland)·1988
Same journal

Structure of C3f, a small peptide specifically released during inactivation of the third component of complement.

Complement (Basel, Switzerland)·1988
Same journal

Effects of anti-C4 antibody on complement production by splenic and peritoneal macrophages.

Complement (Basel, Switzerland)·1988
Same journal

C4-binding protein prevents spontaneous cleavage of C3 in sera of patients with hereditary angioedema.

Complement (Basel, Switzerland)·1988
Same journal

Inhibition of C1q functions by RHP, a protein elevated in sera from patients with rheumatoid arthritis.

Complement (Basel, Switzerland)·1988
Same journal

2nd European Meeting on Complement in Human Disease. September 19-22, 1988, Bari, Italy. Abstracts.

Complement (Basel, Switzerland)·1988
See all related articles

Extracellular calcium (Ca2+) and zinc (Zn2+) ions protect cells from complement-induced damage by preventing membrane leakage, not by inhibiting complement activation. Higher ion concentrations offer greater protection against complement-mediated cell injury.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Antibody-dependent complement activation can lead to cell membrane damage and lysis.
  • The role of specific extracellular cations in modulating complement-mediated cell injury is not fully understood.

Purpose of the Study:

  • To investigate the protective effects of extracellular calcium (Ca2+) and zinc (Zn2+) ions against complement-induced cell membrane damage.
  • To elucidate the mechanism by which Ca2+ and Zn2+ exert their protective effects.

Main Methods:

  • Utilized tonsil lymphocytes and Lettre cells as model systems.
  • Assessed complement-mediated cell permeability changes by measuring lactate dehydrogenase leakage.
  • Quantified the impact of varying Ca2+ and Zn2+ concentrations on complement activation and C9 binding.

Related Experiment Videos

Main Results:

  • Ca2+ and Zn2+ prevented antibody-dependent complement-induced permeability changes in both cell types.
  • Increased Ca2+ and Zn2+ concentrations were required for protection at high complement-to-cell ratios.
  • These ions did not inhibit complement activation or C9 binding but prevented leakage through preformed membrane lesions.

Conclusions:

  • Extracellular Ca2+ concentration directly influences the extent of complement-induced membrane damage.
  • Extracellular Ca2+ and Zn2+ can modulate complement-mediated cell injury by stabilizing the cell membrane against lesion formation.