ApoE(-/-) mice develop atherosclerosis in the absence of complement component C5.
S Patel1, E M Thelander, M Hernandez
1Merck Research Laboratories, 126 East Lincoln Avenue, RY80W-120, Rahway, NJ 07065, USA.
Biochemical and Biophysical Research Communications
|August 4, 2001
Summary
The terminal complement complex does not significantly impact atherosclerosis development in apolipoprotein E-deficient mice. Complement component C5 deficiency did not alter lesion size in this atherosclerosis mouse model.
Area of Science:
- Immunology
- Cardiovascular Research
Background:
- The terminal complex of complement (C5b-9) has been implicated in atherosclerosis pathogenesis.
- Studies in rabbits suggest a role for complement in atherosclerosis, but its role in other models is unclear.
Purpose of the Study:
- To investigate the role of complement component C5 in the development of atherosclerosis in apolipoprotein E-deficient (apoE(-/-)) mice.
Main Methods:
- C5-deficient mice were cross-bred with apoE(-/-) mice.
- Mice were fed a high-fat diet for 22 weeks.
- Aortic root lesion areas were analyzed using morphometric analysis.
Main Results:
- No significant differences in plasma cholesterol or triglyceride levels were observed between apoE(-/-) and apoE(-/-)/C5-deficient mice.
- Morphometric analysis revealed no significant difference in aortic root lesion areas between male and female apoE(-/-) and apoE(-/-)/C5-deficient mice.
Conclusions:
- Complement component C5 deficiency does not significantly affect atherosclerosis development in apoE(-/-) mice.
- Unlike in rabbits, the terminal complement complex does not appear to play a major role in atherosclerosis in this mouse model.
