Circulation. 2001;104:448-454
doi: 10.1161/hc2901.091399
doi: 10.1161/hc2901.091399
(Circulation. 2001;104:448.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
Accelerated Atherosclerosis, Aortic Aneurysm Formation, and Ischemic Heart Disease in Apolipoprotein E/Endothelial Nitric Oxide Synthase Double-Knockout Mice
From the Cardiovascular Research Center, Cardiology Division, and Department of Pathology (T.H.A.), Massachusetts General Hospital, and Harvard Medical School, Boston, Mass.
Correspondence to Paul L. Huang, MD, PhD, Cardiovascular Research Center, Massachusetts General Hospital East, 149 E 13th St, Charlestown, MA 02129. E-mail huangp{at}helix.mgh.harvard.edu
Background— To test whether deficiency in endothelial nitric oxide synthase (eNOS) affects atherosclerosis development, we compared lesion formation in apolipoprotein E (apoE)/eNOS-double knockout (DKO) and apoE-knockout (KO) control animals.
Methods and Results— After 16 weeks of "Western-type" diet, apoE/eNOS-DKO males and females showed significant increases in lesion area of 93.6% and 59.2% compared with apoE-KO mice. All apoE/eNOS-DKO animals studied developed peripheral coronary arteriosclerosis, associated with perivascular and myocardial fibrosis, whereas none of the apoE-KO mice did. Transthoracic echocardiography showed a significantly increased left ventricular wall thickness and decreased fractional shortening in DKO animals. Mean arterial pressure was increased in DKO mice and was comparable in degree to eNOS-KO animals. Male DKO animals developed atherosclerotic abdominal aneurysms and aortic dissection.
Conclusions— eNOS deficiency increases atherosclerosis in Western-type diet-fed apoE-KO animals and introduces coronary disease and an array of cardiovascular complications, including spontaneous aortic aneurysm and dissection. This phenotype constitutes the first murine model to demonstrate distal coronary arteriosclerosis associated with evidence of myocardial ischemia, infarction, and heart failure. Hypertrophy and reduced left ventricular function cannot be explained by increased blood pressure alone, because eNOS-KO animals do not develop these complications.
Key Words: arteriosclerosis • nitric oxide synthase • coronary disease • aneurysm • hypertension
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 P. W Shaul Endothelial nitric oxide synthase, caveolae and the development of atherosclerosis J. Physiol., February 15, 2003; 547(1): 21 - 33. [Abstract] [Full Text] [PDF]
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C. Yan, D. Kim, T. Aizawa, and B. C. Berk Functional Interplay Between Angiotensin II and Nitric Oxide: Cyclic GMP as a Key Mediator Arterioscler Thromb Vasc Biol, January 1, 2003; 23(1): 26 - 36. [Abstract] [Full Text] [PDF]
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J. Chen, P. Kuhlencordt, F. Urano, H. Ichinose, J. Astern, and P. L. Huang L-Arginine on Atherosclerosis in ApoE Knockout and ApoE/Inducible NO Synthase Double-Knockout Mice Arterioscler Thromb Vasc Biol, January 1, 2003; 23(1): 97 - 103. [Abstract] [Full Text] [PDF]
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P B Massion and J-L Balligand Modulation of cardiac contraction, relaxation and rate by the endothelial nitric oxide synthase (eNOS): lessons from genetically modified mice J. Physiol., January 1, 2003; 546(1): 63 - 75. [Abstract] [Full Text] [PDF]
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S. Tateshima, Y. Murayama, J. P. Villablanca, T. Morino, K. Nomura, K. Tanishita, and F. Vinuela In Vitro Measurement of Fluid-Induced Wall Shear Stress in Unruptured Cerebral Aneurysms Harboring Blebs Stroke, January 1, 2003; 34(1): 187 - 192. [Abstract] [Full Text] [PDF]
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R. van Haperen, M. de Waard, E. van Deel, B. Mees, M. Kutryk, T. van Aken, J. Hamming, F. Grosveld, D. J. Duncker, and R. de Crom Reduction of Blood Pressure, Plasma Cholesterol, and Atherosclerosis by Elevated Endothelial Nitric Oxide J. Biol. Chem., December 6, 2002; 277(50): 48803 - 48807. [Abstract] [Full Text] [PDF]
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J. Chen, C.-H. Tung, U. Mahmood, V. Ntziachristos, R. Gyurko, M. C. Fishman, P. L. Huang, and R. Weissleder In Vivo Imaging of Proteolytic Activity in Atherosclerosis Circulation, June 11, 2002; 105(23): 2766 - 2771. [Abstract] [Full Text] [PDF]
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 P. W. M. Fedak, S. Verma, J. Butany, R. D. Weisel, and T. E. David Aortic valve malformations and pulmonary autograft root dilatation J. Thorac. Cardiovasc. Surg., June 1, 2002; 123(6): 1222 - 1223. [Full Text] [PDF]
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J. Wang, D. Dudley, and X. L. Wang Haplotype-Specific Effects on Endothelial NO Synthase Promoter Efficiency: Modifiable by Cigarette Smoking Arterioscler Thromb Vasc Biol, May 1, 2002; 22(5): e1 - 4. [Abstract] [Full Text] [PDF]
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 M. W Manning, L. A Cassis, J. Huang, S. J Szilvassy, and A. Daugherty Abdominal aortic aneurysms: fresh insights from a novel animal model of the disease Vascular Medicine, February 1, 2002; 7(1): 45 - 54. [Abstract] [PDF]
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 C. MINEO and P.W. SHAUL Modulation of Endothelial NO Production by High-density Lipoprotein Cold Spring Harb Symp Quant Biol, January 1, 2002; 67(0): 459 - 470. [Abstract] [PDF]
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J. Chen, P. J. Kuhlencordt, J. Astern, R. Gyurko, and P. L. Huang Hypertension Does Not Account for the Accelerated Atherosclerosis and Development of Aneurysms in Male Apolipoprotein E/Endothelial Nitric Oxide Synthase Double Knockout Mice Circulation, November 13, 2001; 104(20): 2391 - 2394. [Abstract] [Full Text] [PDF]
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W. Shi, X. Wang, D. M. Shih, V. E. Laubach, M. Navab, and A. J. Lusis Paradoxical Reduction of Fatty Streak Formation in Mice Lacking Endothelial Nitric Oxide Synthase Circulation, April 30, 2002; 105(17): 2078 - 2082. [Abstract] [Full Text] [PDF]
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