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Updated: Feb 8, 2026
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Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
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Lipocalin-2 contributes to experimental atherosclerosis in a stage-dependent manner
J Amersfoort1, F H Schaftenaar1, H Douna1
1Division of Biotherapeutics, LACDR, Leiden University, Einsteinweg 55, 2333CC, Leiden, The Netherlands.
Atherosclerosis
|July 2, 2018
Summary
Lipocalin-2 (Lcn2) deficiency accelerates early atherosclerosis lesion growth but reduces necrotic core size and MMP-9 activity in advanced lesions, impacting plaque stability.
Area of Science:
- Biochemistry
- Immunology
- Cardiovascular Research
Background:
- Lipocalin-2 (Lcn2) is an immune-secreted glycoprotein implicated as a biomarker for unstable atherosclerotic lesions.
- Lcn2 is known to interact with matrix metalloproteinase-9 (MMP-9), suggesting a role in plaque development.
Purpose of the Study:
- To investigate the functional role of Lcn2 in various stages of atherosclerosis.
- To determine the impact of Lcn2 deficiency on atherosclerotic lesion progression and stability.
Main Methods:
- Generation of Ldlr-/-Lcn2-/- mice to model atherosclerosis.
- Histological analysis of atherosclerotic lesions.
- Flow cytometry to examine myeloid cell populations, particularly inflammatory monocytes.
Main Results:
- Ldlr-/-Lcn2-/- mice exhibited larger atherosclerotic lesions in early stages.
- Increased circulating Ly6Chi inflammatory monocytes were observed in Lcn2-deficient mice.
- Diminished MMP-9 activity and reduced necrotic core area in advanced lesions of Ldlr-/-Lcn2-/- mice.
Conclusions:
- Lcn2 deficiency promotes early lesion growth in atherosclerosis.
- Lcn2 deficiency impacts advanced lesion stability by decreasing MMP-9 activity and necrotic core size.
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