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Updated: Feb 8, 2026

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
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.
Background And Aims:
Lipocalin-2 (Lcn2) is a glycoprotein which can be secreted by immune cells. Several studies in humans have suggested Lcn2 can be used as a biomarker for the detection of unstable atherosclerotic lesions, partly as it is known to interact with MMP-9.
Methods:
In this study, we generated Ldlr-/-Lcn2-/- mice to assess the functional role of Lcn2 in different stages of atherosclerosis. Atherosclerotic lesions were characterized through histological analysis and myeloid cell populations were examined using flow cytometry.
Results:
We show that Ldlr-/-Lcn2-/- mice developed larger atherosclerotic lesions during earlier stages of atherosclerosis and had increased circulating Ly6Chi inflammatory monocytes compared to Ldlr-/- mice. Advanced atherosclerotic lesions from Ldlr-/-Lcn2-/- mice had decreased necrotic core area, suggesting Lcn2 deficiency may affect lesion stability. Furthermore, MMP-9 activity was diminished in plaques from Ldlr-/-Lcn2-/- mice.
Conclusions:
Altogether, these findings suggest that Lcn2 deficiency promotes lesion growth in earlier stages of the disease while it decreases MMP-9 activity and necrotic core size in advanced atherosclerosis.
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