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ReductionofAMP-ActivatedProteinKinaseα2Increases
Reduction of AMP-Activated Protein Kinase α2 Increases Endoplasmic Reticulum Stress and Atherosclerosis In Vivo by Yunzhou Dong, Miao Zhang, Bin Liang, Zhonglin Xie, Zhengxing Zhao, Sima Asfa, Hyoung Chul Choi, and Ming-Hui Zou Circulation Volume 121(6):792-803 February 16, 2010 Copyright ? American Heart Association, Inc. All rights reserved. Figure 1. Reduction of AMPKα2 expression induces ER stress in endothelial cells. Yunzhou Dong et al. Circulation. 2010;121:792-803 Copyright ? American Heart Association, Inc. All rights reserved. Figure 2. AMPKα2-dependent ER stress in isolated MAECs. A, Characterization of MAECs from WT, AMPKα1 KO, and AMPKα2 KO. AMPKα, AMPKα1, and AMPKα2 were detected by use of the specific antibodies in Western blots. Yunzhou Dong et al. Circulation. 2010;121:792-803 Copyright ? American Heart Association, Inc. All rights reserved. Figure 3. AMPKα deletion causes a calcium-dependent ER stress response in endothelial cells. Yunzhou Dong et al. Circulation. 2010;121:792-803 Copyright ? American Heart Association, Inc. All rights reserved. Figure 4. AMPK inhibition impairs ionomycin-induced Ca2+ release and return transients. Yunzhou Dong et al. Circulation. 2010;121:792-803 Copyright ? American Heart Association, Inc. All rights reserved. Figure 5. SERCA-mediated ER stress in MAECs from AMPKα2?/? mice. Yunzhou Dong et al. Circulation. 2010;121:792-803 Copyright ? American Heart Association, Inc. All rights reserved. Figure 6. AMPKα2 deletion inhibits SERCA activity but increases its oxidation status in endothelial cells. Yunzhou Dong et al. Circulation. 2010;121:792-803 Copyright ? American Heart Association, Inc. All rights reserved. Figure 7. Increased atherosclerosis in the aortic roots of LDLr?/?/AMPKα2?/? mice. Yunzhou Dong et al. Circulation. 2010;121:792-803 Copyright ? American Heart Association, Inc. All rights reserved. Figure 8. Long-term administration of TUDCA reduces ER stress and aortic lesions in mice deficient for bot
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