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Published on: November 17, 2018
[The effect of atorvastatin on the expression of CD55, CD59 in patients with hyperlipidemia]
Yong-ming Liu1, Jin-chun He, Jing-gang Yang
1Department of Gerontology, First Hospital, Lanzhou University, Lanzhou 730000, China. cardtonm@263.net
Insights
CD55 expression is reduced in hyperlipidemia, linked to inflammation and obesity, not blood lipids. Atorvastatin therapy increases CD59 expression, independent of lipid changes.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Pharmacology
Background:
- Hyperlipidemia is associated with an increased risk of cardiovascular disease.
- Complement regulatory proteins CD55 and CD59 play roles in immune responses and inflammation.
- Understanding their role in hyperlipidemia may offer therapeutic insights.
Purpose of the Study:
- To investigate the expression levels of CD55 and CD59 in patients with hyperlipidemia.
- To evaluate the impact of atorvastatin on CD55 and CD59 expression.
- To identify factors influencing these protein expressions in hyperlipidemia.
Main Methods:
- Flow cytometry was used to measure CD55 and CD59 on white blood cells in 67 hyperlipidemia patients and 24 controls.
- Correlations with blood lipids, complement activation markers (C5a, sC5b-9), and inflammatory factors (hsCRP, TNF-alpha, IL-6) were analyzed.
- 24 hyperlipidemia patients received atorvastatin for 8-12 weeks, with protein expressions measured pre- and post-treatment.
Main Results:
- CD55 expression on lymphocytes and monocytes was significantly lower in hyperlipidemia patients compared to controls.
- CD55 expression negatively correlated with waist circumference, hsCRP, and C5a levels.
- Atorvastatin treatment increased CD59 expression on lymphocytes, monocytes, and granulocytes, irrespective of lipid level changes.
Conclusions:
- CD55 expression is down-regulated in hyperlipidemia, potentially influenced by obesity and inflammation, but not directly by blood lipid levels.
- CD55 expression is linked to complement activation pathways.
- Atorvastatin therapy up-regulates CD59 expression in hyperlipidemia patients independently of its lipid-lowering effects.
Objective:
To study the expressions of CD55 and CD59 in patients with hyperlipidemia and the effects of atorvastatin on it, and to identify the possible influential factors.
Methods:
We selected 67 patients with hyperlipidemia, and 24 healthy people matched in terms of age, sex and body weight as control. The expressions of CD55 and CD59 on white blood cells were detected by flow cytometry, and their relationships to blood lipids, complement activation indexes (C(5a), sC(5b-9)), inflammatory factors (high sensitivity C-reactive protein (hsCRP), TNF-alpha, IL-6 were analyzed. 24 patients with hyperlipidemia were treated with atorvastatin for 8-12 weeks and the expressions of CD55 and CD59 were measured before and after atorvastatin therapy.
Results:
The mean fluorescence intensity (MFI) of CD55 lymphocytes and monocytes were decreased in patients with hyperlipidemia compared with control (2.07 +/- 0.28 vs 2.29 +/- 0.44 and 3.45 +/- 1.02 vs 4.33 +/- 2.32, P < 0.01 and P < 0.05, respectively). CD55 positive lymphocyte MFI was negatively correlated with waist circumference, waist-hip ratio, hsCRP and C(5a). C(5a) was negatively correlated with the MFIs of CD55 positive lymphocytes, monocytes, granulocytes, and positively with TG and diastolic blood pressure. After atorvastatin therapy, the MFIs of CD59 positive lymphocytes, monocytes and granulocytes increased (4.34 +/- 1.16 vs 3.69 +/- 0.76, 4.52 +/- 1.36 vs 3.91 +/- 0.89, 5.67 +/- 1.72 vs 4.56 +/- 1.03, P < 0.05, < 0.05 and < 0.01 respectively), which were not correlated with changes of blood lipids.
Conclusions:
The expression of CD55 is down-regulated in hyperlipidemia, which might be influenced by obesity, abdominal distribution of adipose tissue and inflammatory status of hyperlipidemia, but not by blood lipids. The expression of CD55 is related with complement activation; The expression of CD59 is up-regulated after atorvastatin treatment independently of blood lipids.
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