Dataset Information

Accelerated atherogenesis in completely ligated common carotid artery of apolipoprotein E-deficient mice.

ABSTRACT: Complete ligation of the common carotid artery near its bifurcation induces neointimal formation due to smooth muscle cell proliferation in normolipidemic wild-type mice, but it was unknown what would happen to hyperlipidemic apolipoprotein E-deficient (Apoe-/-) mice. Examination of these mice revealed rapid development of atherosclerotic lesions in completely ligated carotid arteries within 4 weeks. Mice were fed a Western diet, starting 1 week before ligation, or a chow diet. Foam cell lesions formed as early as 1 week after ligation in mice fed the Western diet and 2 weeks in mice fed the chow diet. Fibrous lesions comprised of foam cells and smooth muscle cells and more advance lesions containing neovessels occurred at 2 and 4 weeks after ligation, respectively, in the Western diet group. Lesions were larger and more advanced in the Western diet group than the chow group. Neutrophil infiltration was observed in growing intimal lesions in both diet groups, while CD8+ T cells were found in lesions of chow-fed mice. This study demonstrates that Apoe-/- mice develop the entire spectrum of atherosclerosis in ligated carotid arteries in an accelerated manner and this model could be a valuable tool for investigating the development and therapy of atherosclerosis.

SUBMITTER: Chang Z

PROVIDER: S-EPMC5746382 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Accelerated atherogenesis in completely ligated common carotid artery of apolipoprotein E-deficient mice.

Chang Zhihui Z Huangfu Chaoji C Grainger Andrew T AT Zhang Jingang J Guo Qiyong Q Shi Weibin W

Oncotarget 20171125 66

Complete ligation of the common carotid artery near its bifurcation induces neointimal formation due to smooth muscle cell proliferation in normolipidemic wild-type mice, but it was unknown what would happen to hyperlipidemic apolipoprotein E-deficient (Apoe<sup>-/-</sup>) mice. Examination of these mice revealed rapid development of atherosclerotic lesions in completely ligated carotid arteries within 4 weeks. Mice were fed a Western diet, starting 1 week before ligation, or a chow diet. Foam c ...[more]

PMID: 29299147

Similar Datasets

Project description:microRNA-155 (miR155) plays a critical role in immunity and macrophage inflammation. We aim to investigate the role of miR155 in atherogenesis.Quantitative real-time polymerase chain reaction showed that miR155 was expressed in mouse and human atherosclerotic lesions. miR155 expression in macrophages was correlated positively with proinflammatory cytokine expression. Lentivirus-mediated overexpression of miR155 in macrophages enhanced their inflammatory response to lipopolysaccharide through targeting suppressor of cytokine signaling-1 and impaired cholesterol efflux from acetylated low-density lipoprotein-loaded macrophages, whereas deficiency of miR155 blunted macrophage inflammatory responses and enhanced cholesterol efflux possibly via enhancing lipid loading-induced macrophage autophagy. We next examined the atherogenesis in apolipoprotein E-deficient (apoE(-/-)) and miR155(-/-)/apoE(-/-) (double knockout) mice fed a Western diet. Compared with apoE(-/-) mice, the double knockout mice developed less atherosclerosis lesion in aortic root, with reduced neutral lipid content and macrophages. Flow cytometric analysis showed that there were increased number of regulatory T cells and reduced numbers of Th17 cells and CD11b+/Ly6C(high) cells in the spleen of double knockout mice. Peritoneal macrophages from the double knockout mice had significantly reduced proinflammatory cytokine expression and secretion both in the absence and presence of lipopolysaccharide stimulation. To determine whether miR155 in leukocytes contributes to atherosclerosis, we performed a bone marrow transplantation study. Deficiency of miR155 in bone marrow-derived cells suppressed atherogenesis in apoE(-/-) mice, demonstrating that hematopoietic cell-derived miR155 plays a critical role.miR155 deficiency attenuates atherogenesis in apoE(-/-) mice by reducing inflammatory responses of macrophages, enhancing macrophage cholesterol efflux and resulting in an antiatherogenic leukocyte profile. Targeting miR155 may be a promising strategy to halt atherogenesis.

Dataset Information

Accelerated atherogenesis in completely ligated common carotid artery of apolipoprotein E-deficient mice.

Publications

Accelerated atherogenesis in completely ligated common carotid artery of apolipoprotein E-deficient mice.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets