Apelin/APJ Signaling Is a Critical Regulator of Statin Effects in Vascular Endothelial Cells-Brief Report
- Authors
- McLean, Danielle L.; Kim, Jongmin; Kang, Yujung; Shi, Hong; Atkins, G. Brandon; Jain, Mukesh K.; Chun, Hyung J.
- Issue Date
- Nov-2012
- Publisher
- LIPPINCOTT WILLIAMS WILKINS
- Citation
- ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, v.32, no.11, pp 2640 - 2640
- Pages
- 1
- Journal Title
- ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
- Volume
- 32
- Number
- 11
- Start Page
- 2640
- End Page
- 2640
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/147558
- DOI
- 10.1161/ATVBAHA.112.300317
- ISSN
- 1079-5642
1524-4636
- Abstract
- Objective-The endothelial response elicited by the G-protein-coupled receptor pathway involving apelin and APJ predicts an overall vasoprotective effect. As a number of downstream endothelial targets of apelin/APJ signaling are also known to be targeted by statins (3-hydroxy-3-methyl-glutaryl [HMG]-CoA reductase inhibitors) as potential mediators of their known pleiotropic effects, we evaluated for the involvement of apelin/APJ signaling in statin endothelial effects.
Methods and Results-We found that disruption of apelin/APJ signaling in endothelial cells leads to significantly decreased expression of Kruppel-like factor 2, endothelial nitric oxide synthase, and thrombomodulin. We found that statin-mediated induction of Kruppel-like factor 2, endothelial nitric oxide synthase, and thrombomodulin expression, as well as inhibition of monocyte-endothelial adhesion, was abrogated by concurrent apelin knockdown. Moreover, we found that statins can transcriptionally regulate APJ in a Kruppel-like factor 2-dependent manner, demonstrating the presence of a positive-feedback loop.
Conclusion-Our findings provide a novel mechanism by which the apelin/APJ pathway serves as a critical intermediary that links statin to its pleiotropic effects in regulating endothelial gene targets and function. (Arterioscler Thromb Va
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