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Protease-Activated Receptor-2 Deficiency Attenuates Atherosclerotic Lesion Progression and Instability in Apolipoprotein E-Deficient Mice.
Zuo, Pengfei; Zuo, Zhi; Zheng, Yueyue; Wang, Xin; Zhou, Qianxing; Chen, Long; Ma, Genshan.
Afiliação
  • Zuo P; Department of Cardiology, Zhongda Hospital Affiliated to Southeast UniversityNanjing, China.
  • Zuo Z; Department of Cardiology, Zhongda Hospital Affiliated to Southeast UniversityNanjing, China.
  • Zheng Y; Department of Cardiology, Zhongda Hospital Affiliated to Southeast UniversityNanjing, China.
  • Wang X; Department of Cardiology, Zhongda Hospital Affiliated to Southeast UniversityNanjing, China.
  • Zhou Q; Department of Cardiology, Zhongda Hospital Affiliated to Southeast UniversityNanjing, China.
  • Chen L; Department of Cardiology, Zhongda Hospital Affiliated to Southeast UniversityNanjing, China.
  • Ma G; Department of Cardiology, Zhongda Hospital Affiliated to Southeast UniversityNanjing, China.
Front Pharmacol ; 8: 647, 2017.
Article em En | MEDLINE | ID: mdl-28959204
Inflammatory mechanisms are involved in the process of atherosclerotic plaque formation and rupture. Accumulating evidence suggests that protease-activated receptor (PAR)-2 contributes to the pathophysiology of chronic inflammation on the vasculature. To directly examine the role of PAR-2 in atherosclerosis, we generated apolipoprotein E/PAR-2 double-deficient mice. Mice were fed with high-fat diet for 12 weeks starting at ages of 6 weeks. PAR-2 deficiency attenuated atherosclerotic lesion progression with reduced total lesion area, reduced percentage of stenosis and reduced total necrotic core area. PAR-2 deficiency increased fibrous cap thickness and collagen content of plaque. Moreover, PAR-2 deficiency decreased smooth muscle cell content, macrophage accumulation, matrix metallopeptidase-9 expression and neovascularization in plaque. Relative quantitative PCR assay using thoracic aorta revealed that PAR-2 deficiency reduced mRNA expression of inflammatory molecules, such as vascular cell adhesion molecule-1, intercellular adhesion molecule-1, tumor necrosis factor (TNF)-α and monocyte chemoattractant protein (MCP)-1. In vitro experiment, we found that PAR-2 deficiency reduced mRNA expression of interferon-γ, interleukin-6, TNF-α and MCP-1 in macrophage under unstimulated and lipopolysaccharide-stimulated conditions. These results suggest that PAR-2 deficiency attenuates the progression and instability of atherosclerotic plaque.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2017 Tipo de documento: Article