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Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Altered gene expression in early atherosclerosis is blocked by low level apolipoprotein E
Yanqing Ma1, Craig C Malbon, David L Williams
1Department of Pharmacological Sciences, School of Medicine, Stony Brook University, Stony Brook, New York, United States of America.
Plos One
|June 19, 2008
Summary
Apolipoprotein E (apoE(-/-))) deficiency accelerates atherosclerosis in mice, increasing inflammatory molecules. Low-level apoE expression is atheroprotective, reducing lesions and molecular changes.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Atherosclerosis Research
Background:
- Mice lacking apolipoprotein E (apoE(-/-)) spontaneously develop atherosclerosis.
- Investigating the link between adhesion molecules and atherosclerosis is crucial for understanding disease progression.
- The study explores whether expressing low levels of apolipoprotein E can prevent lesion formation.
Purpose of the Study:
- To determine the role of adhesion molecules and inflammatory markers in apoE(-/-) mouse atherosclerosis.
- To investigate the therapeutic potential of low-level apolipoprotein E expression in preventing atherosclerosis.
Main Methods:
- Analysis of mRNA and protein expression of adhesion molecules (LFA-1, MAC-1, VCAM-1, ICAM-1, CD44) and inflammatory markers (MCP-1, cathepsin B, COX-2) in atherosclerotic aortas of apoE(-/-) mice.
- Assessment of aortic lesion formation in apoE(-/-) mice with and without very low levels of transgenic apolipoprotein E expression.
Main Results:
- Elevated mRNA expression of adhesion molecules and inflammatory markers was observed in atherosclerotic aortas of apoE(-/-) mice at various ages.
- Protein levels of CD11a, VCAM-1, and cathepsin B were also increased in apoE(-/-) aortas.
- Suppression of aortic lesions and normalization of key molecular markers were achieved by expressing low levels of transgenic apolipoprotein E.
Conclusions:
- Atherosclerotic lesions are detectable in apoE(-/-) mice as early as 4 weeks of age.
- Low-level apolipoprotein E expression demonstrates significant atheroprotective effects.
- Apolipoprotein E expression effectively suppresses the upregulation of adhesion and inflammatory molecules in early atherosclerotic lesions.
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