| First Author | Liu M | Year | 2017 |
| Journal | Int J Mol Sci | Volume | 18 |
| Issue | 3 | PubMed ID | 28300760 |
| Mgi Jnum | J:287606 | Mgi Id | MGI:6415466 |
| Doi | 10.3390/ijms18030644 | Citation | Liu M, et al. (2017) The Essential Role of Pin1 via NF-kappaB Signaling in Vascular Inflammation and Atherosclerosis in ApoE(-/-) Mice. Int J Mol Sci 18(3):644 |
| abstractText | Atherosclerosis, as a chronic inflammatory disease, is the major underlying cause of death worldwide. However, the mechanisms that underlie the inflammatory process are not completely understood. Prolyl-isomerase-1 (Pin1), as a unique peptidyl-prolyl isomerase, plays an important role in inflammation and endothelial dysfunction. Herein, we investigate whether Pin1 regulates vascular inflammation and atherosclerosis, and clarify its mechanisms in these processes. ApoE(-/-) mice were randomly given either juglone (0.3, 1 mg/kg, two times per week) or vehicle i.p. for 4 weeks. Compared with ApoE(-/-) mice, treatment by juglone resulted not only in markedly attenuated macrophage infiltration and atherosclerotic lesion area in a lipid-independent manner, but also in decreased expression of Pin1, vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), and NF-kappaB activity in aorta. Then, EA.hy926 cells were pretreated with juglone (6 mumol/L), Pin1 siRNA, NF-kappaB inhibitor, or vehicle prior to exposure to ox-LDL (50 mug/mL). It was observed that treatment with juglone or Pin1 siRNA suppressed expression of VCAM-1 in oxLDL-incubated EA.hy926 cells and decreased THP-1 cell adhesion to oxLDL-stimulated endothelial cells through the NF-kappaB signal pathway. Our findings indicate that Pin1 plays a vital role on the development of vascular inflammation and atherosclerosis. |
