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Pathological and molecular analyses of atherosclerotic lesions in ApoE-knockout mice

Shibata, Masa-Aki ; Shibata, Eiko ; Maemura, Kentaro ; Kondo, Yoichi ; Harada-Shiba, Mariko

Medical molecular morphology, 2017-09, Vol.50 (3), p.130-144 [Periódico revisado por pares]

Tokyo: Springer Japan

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Título:
Pathological and molecular analyses of atherosclerotic lesions in ApoE-knockout mice
Autor: Shibata, Masa-Aki ; Shibata, Eiko ; Maemura, Kentaro ; Kondo, Yoichi ; Harada-Shiba, Mariko
Assuntos: Anatomy ; Animals ; Apolipoprotein E ; Apolipoproteins E - deficiency ; Apolipoproteins E - metabolism ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - blood ; Atherosclerosis - diagnostic imaging ; Atherosclerosis - genetics ; Atherosclerosis - pathology ; Carotid Intima-Media Thickness ; Chemokines ; CXCL16 protein ; Formaldehyde ; Gelatinase B ; High fat diet ; Immunohistochemistry ; Inflammation ; Lesions ; Lipids - blood ; Liquid oxygen ; LOX-1 protein ; Macrophages ; Male ; Matrix Metalloproteinases - metabolism ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular biology ; Molecular Medicine ; Molecular modelling ; Neutrophil collagenase ; Original Paper ; Paraffin ; Pathology ; Polymerase chain reaction ; Proteins ; Real-Time Polymerase Chain Reaction ; Rodents ; Scavenger Receptors, Class E ; Tenascin ; Tenascin C ; Tissue inhibitor of metalloproteinase 1 ; Tissues
É parte de: Medical molecular morphology, 2017-09, Vol.50 (3), p.130-144
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Descrição: The establishment of consistent and reliable methods for the analysis of atherosclerosis molecular pathways and for testing the efficiency of new therapeutics is of utmost importance. Here, we fed ApoE -knockout (KO) mice with high-fat diet to for 16 weeks to induce atherosclerosis. Atherosclerotic lesions in mice were methodically investigated using pathologic analyses and molecular biology tools. These lesions were histopathologically classified into three categories: early, progressive, and combined lesions. Immunohistochemical analyses showed that both F4/80 (macrophage marker) and tenascin-C are expressed in these lesions. Real-time PCR analysis conducted using formalin-fixed paraffin-embedded tissues with atherosclerotic lesions demonstrated an increase in the levels of many inflammatory chemokines, including Cxcl16 , while antibody arrays performed using frozen atherosclerotic tissue samples showed elevated TIMP-1 expression. Subsequent immunohistochemical analyses showed that the expression of CXCL16, TIMP-1, MMP-9, MMP-8, and LOX-1 is localized in the atherosclerotic lesions. We confirmed that the expression of these proteins is localized to atherosclerotic lesion, which suggests their roles in the development of the lesions in ApoE -KO mice. Therefore, this mouse model represents an appropriate tool for elucidating molecular mechanisms underlying the development of atherosclerosis, and a model for the evaluation of therapeutic efficiency of novel drugs.
Editor: Tokyo: Springer Japan
Idioma: Inglês

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