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Published on: July 1, 2011
Complement activation in the arteries of patients with severe atherosclerosis
Xiaowen Ge1, Chen Xu1, Yalan Liu1
1Department of Pathology, Zhongshan Hospital, Fudan University Shanghai, P. R. China.
Insights
Complement activation, indicated by C3b/iC3b and membrane attack complex (MAC) deposition, is linked to atherosclerosis (AS). Higher levels correlate with hypertension and hypertriglyceridemia, suggesting a role in AS development.
Area of Science:
- Immunology
- Cardiovascular Disease
- Pathogenesis of Atherosclerosis
Background:
- Excessive complement system activation is implicated in atherosclerosis (AS) pathogenesis.
- Investigated complement activation in AS lesions by detecting C3b/iC3b and membrane attack complex (MAC) deposition.
- Analyzed correlations between complement deposition levels and patient clinicopathological features.
Purpose of the Study:
- To determine if complement is activated in atherosclerotic arteries.
- To quantify C3b/iC3b and MAC deposition in AS lesions.
- To explore the relationship between complement activation markers and clinical characteristics of AS patients.
Main Methods:
- Immunohistochemistry (IHC) used to evaluate C3b/iC3b and MAC deposition in 79 AS patients.
- Deposition levels were scored and correlated with recorded clinical features.
- Comparison made between AS arteries and normal arteries.
Main Results:
- Significantly increased C3b/iC3b and MAC deposits observed in AS arteries versus normal arteries.
- Higher C3b/iC3b deposition correlated with a greater prevalence of hypertension.
- Increased MAC deposition was associated with a higher prevalence of hypertriglyceridemia.
Conclusions:
- C3b/iC3b and MAC deposition confirm complement activation in atherosclerotic arteries.
- Elevated deposition suggests excessive complement activation contributes to AS development.
- Hypertension and hypertriglyceridemia may be linked to complement C3 activation and MAC formation, respectively.
Background:
Excessive complement activation plays an important role in the pathogenesis of atherosclerosis (AS). We therefore wanted to investigate whether complement is activated in areas of AS by detecting the deposition of C3b/iC3b and membrane attack complex (MAC). We also analyzed the relationships between C3b/iC3b and MAC levels and the clinicopathological features of patients with AS.
Methods:
The sample comprised 79 patients who had been diagnosed with AS. Their levels of C3b/iC3b and MAC deposition were evaluated by immunohistochemistry (IHC). The results were translated into scores, and the patients' clinical features were recorded.
Results:
Compared with normal arteries, significantly greater deposits of C3b/iC3b and MAC were found in AS arteries. In the group with more C3b/iC3b deposition, the ratio of patients with hypertension was higher. Moreover, in the group with more MAC deposition, the ratio of patients with hypertriglyceridemia was higher.
Conclusions:
The finding of C3b/iC3b and MAC deposition in atherosclerotic arteries points to the activation of complement. Greater amounts of C3b/iC3b and MAC deposition imply excessive complement activation, which can lead to the development of AS. Hypertension and hypertriglyceridemia may, respectively, contribute to the activation of complement C3 or the formation of MAC.
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