alexa Gene Therapy Targeting LDL Cholesterol but not HDL Chol
ISSN: 2157-7412

Journal of Genetic Syndromes & Gene Therapy
Open Access

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Research Article

Gene Therapy Targeting LDL Cholesterol but not HDL Cholesterol Induces Regression of Advanced Atherosclerosis in a Mouse Model of Familial Hypercholesterolemia

Rongying Li1, Hsu Chao2, Kerry W.S. Ko2, Shelley Cormier2, Carrie Dieker2, Elie A. Nour2, Shining Wang2, Lawrence Chan1,2 and Kazuhiro Oka1,2*

1Department of Medicine,Baylor College of Medicine, Houston, TX 77030

2Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

*Corresponding Author:
Kazuhiro Oka
Department of Molecular & Cellular Biology
Baylor College of Medicine, BCM130
One Baylor Plaza, Houston, TX 77030
Tel: 713-7D98-7381
Fax: 713-798-8764
E-mail: [email protected]

Received date: September 12, 2011; Accepted date:September 22, 2011; Published date: September 28, 2011

Citation: Li R, Chao H, Ko KWS, Cormier S, Dieker C, et al. (2011) Gene TherapyTargeting LDL Cholesterol but not HDL Cholesterol Induces Regression of Advanced Atherosclerosis in a Mouse Model of Familial Hypercholesterolemia. J Genet Syndr Gene Ther 2:106. doi:10.4172/2157-7412.1000106

Copyright: © 2011 Li R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse, distribution, and reproduction in any medium, provided the original author and source are credited.



A reduction in low density lipoprotein (LDL) cholesterol or an increase in high density lipoprotein (HDL) cholesterol can reduce the risk of development of atherosclerosis through overlapping, or independent mechanisms. However, the clinical outcome of combined therapy remains in debate. In this study, we first characterized effects of various constructs of helper-dependent adenoviral vector (HDAd) expressing apolipoprotein E3 or LDL receptor (LDLR) in vivo on plasma cholesterol levels. Using this information, we designed experiments and compared the effects of long-term (28 weeks) LDL cholesterol lowering or raising HDL cholesterol, or a combination of both on advanced atherosclerosis in Ldlr?/?mice, a mouse model of familial hypercholesterolemia. Our major findings are: (i) various factors influence in vivo functional activity, which appear to be context dependent; (ii) apolipoprotein AI (APOAI) gene transfer, which raises HDL cholesterol, retards progression of atherosclerosis but does not induce regression; (iii) LDLR or LDLR and APOAI combination gene therapy induces lesion regression; however, LDLR gene transfer accounts for the majority of the effects of combined gene therapy; (iv) LDLR gene therapy reduces interleukin-7, which is a master regulator of T-cell homeostasis, but APOAI gene therapy does not. These results indicate that LDL cholesterol lowering is effective and sufficient in protection against atherosclerosis and induction of regression of pre-existing atherosclerosis.


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