| First Author | Amersfoort J | Year | 2018 |
| Journal | Atherosclerosis | Volume | 275 |
| Pages | 214-224 | PubMed ID | 29960897 |
| Mgi Jnum | J:324958 | Mgi Id | MGI:6859868 |
| Doi | 10.1016/j.atherosclerosis.2018.06.015 | Citation | Amersfoort J, et al. (2018) Lipocalin-2 contributes to experimental atherosclerosis in a stage-dependent manner. Atherosclerosis 275:214-224 |
| abstractText | 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 Ly6C(hi) 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. |
