| Autor: |
Dyah W. Anggrahini, Noriaki Emoto, Kazuhiko Nakayama, Bambang Widyantoro, Suko Adiarto, Naoko Iwasa, Hidemi Nonaka, Yoshiyuki Rikitake, Yaz Y. Kisanuki, Masashi Yanagisawa, Ken-ichi Hirata |
| Předmět: |
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| Zdroj: |
Cardiovascular Research; Apr2009, Vol. 82 Issue 1, p143-143, 1p |
| Abstrakt: |
Aims Although endothelin-1 (ET-1) has been suggested to contribute to the pathogenesis of neointima formation and atherosclerosis, the individual roles of ET-1 derived from certain cell types in this disease remain unclear. In this study, we determined the role of vascular endothelial ET-1 on vascular inflammation and neointima formation using vascular endothelial ET-1-knockout [ET-1f/f; Tie2-Cre (+)] mice. Methods and results Intimal hyperplasia was induced by complete ligation of the left carotid artery in 12-week-old male ET-1f/f;Tie2-Cre (+) mice (n = 35) and the wild-type (WT) littermates (n = 34). Following this intervention, neointima formation was reduced in ET-1f/f;Tie2-Cre (+) mice compared with the WT mice, independent of the difference in blood pressure. This reduction was associated with a decrease in inflammatory cell recruitment to the vessel wall, which was accompanied by reduced expression levels of endothelial adhesion molecules as well as chemokines and a decrease in vascular smooth muscle cell proliferation. Conclusion The results of our study provide direct evidence for the role of vascular endothelial ET-1 in mediating vascular inflammation and neointima formation following vascular injury in addition to promoting vasoconstriction and cell proliferation. Furthermore, this study suggests a strategy for the efficient design of ET receptor antagonists with targeted inhibition of ET-1 signalling in vascular endothelial cells. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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