期刊
GENETICS AND MOLECULAR RESEARCH
卷 14, 期 4, 页码 14871-14881出版社
FUNPEC-EDITORA
DOI: 10.4238/2015.November.18.52
关键词
Apolipoprotein E-knockout mice; Plaque vulnerability; Pristane; Systemic lupus erythematosus; Type I interferon
资金
- National Natural Science Foundation of China [81373207, 81102267]
- Special Fund for Public Benefit Research from the Ministry of Health [201202004]
- Shanghai Municipal Education Commission [12YZ055]
- Special Research Foundation for the Doctoral Program of Higher Education [201100731120091]
- Training and Subsidization Program for Young Teachers of Shanghai Colleges and Universities
This study aimed to investigate the relationship between type I interferon (IFN-I) and plaque stability in pristane-treated apolipoprotein E-knockout (ApoE(-/-)) mice. Antinuclear antibody (ANA) and extractable nuclear antigen antibody (ENA) levels were measured by immunofluorescence and enzyme-linked immunospot assay. Atherosclerotic plaques were detected by Sirius red/fast green staining. Cell apoptosis was detected by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick-end labeling. Gene expression was determined by real-time PCR analyses. We found that pristane-treated ApoE(-/-) mice developed a lupus-like syndrome characterized by an increased production of serum ANA and ENA. Pristane treatment decreased the collagen content and increased the number of apoptotic cells in plaques. Moreover, IFN-induced ISG15, IFIT1-1, and IFIT1-2 gene expression was increased in peripheral blood cells and aortic plaques. An IFN-alpha-stimulated macrophage supernatant inhibited collagen type I, alpha 1 gene expression in vascular smooth muscle cells. We concluded that the vulnerability of plaques was associated with the activation of IFN-I in pristane-treated ApoE(-/-) mice. Thus, we speculated that the higher prevalence of cardiovascular events in patients with systemic lupus erythematosus could be due to plaque instability.
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