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Related Experiment Video

Updated: Jun 26, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Complement regulator CD59 protects against atherosclerosis by restricting the formation of complement membrane attack

Gongxiong Wu¹, Weiguo Hu, Aliakbar Shahsafaei

¹Department of Medicine, Brigham and Women's Hospital, Laboratory forTranslational Research, Harvard Medical School, Cambridge, MA 02139, USA.

Circulation Research

|January 10, 2009

Summary

Loss of CD59 accelerates atherosclerosis in mice lacking apolipoprotein E, increasing plaque vulnerability and mortality. Complement inhibition and CD59 overexpression show protective effects, suggesting therapeutic potential for atherosclerosis.

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Last Updated: Jun 26, 2026

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Area of Science:

Immunology
Cardiovascular Research
Molecular Biology

Background:

Complement system is crucial in immunity and inflammation.
CD59 regulates complement Membrane Attack Complex (MAC) formation.
The role of terminal complement in atherosclerosis is not fully understood.

Purpose of the Study:

To investigate the role of CD59 in atherosclerosis development.
To determine the atherogenic potential of MAC.
To explore CD59 as a therapeutic target for atherosclerosis.

Main Methods:

Generated mice deficient in both murine CD59 and apolipoprotein E (mCd59ab(-/-)/ApoE(-/-)).
Assessed atherosclerosis progression, plaque characteristics, and survival.
Utilized endothelial overexpression of human CD59 and complement inhibition (anti-mouse C5 antibody).

Main Results:

Loss of CD59 accelerated advanced atherosclerosis, leading to occlusive coronary lesions, vulnerable plaques, and premature death.
Overexpression of human CD59 in the endothelium attenuated these effects.
Complement inhibition reduced atherosclerosis in mCd59ab(-/-)/ApoE(-/-) mice.
MAC mediated endothelial damage and foam cell formation.

Conclusions:

Terminal complement, specifically MAC, plays an atherogenic role.
CD59 exhibits atheroprotective functions.
Inhibiting MAC formation represents a potential therapeutic strategy for atherosclerosis.