APA
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Ben-Aicha, S., Casaní, L., Muñoz-García, N., Joan-Babot, O., Peña, E., Aržanauskaitė, M., … Vilahur, G. (2020). HDL (High-Density Lipoprotein) Remodeling and Magnetic Resonance Imaging–Assessed Atherosclerotic Plaque Burden. Arteriosclerosis, Thrombosis, and Vascular Biology.
Chicago/Turabian
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Ben-Aicha, S., L. Casaní, Natàlia Muñoz-García, Oriol Joan-Babot, E. Peña, M. Aržanauskaitė, M. Gutierrez, et al. “HDL (High-Density Lipoprotein) Remodeling and Magnetic Resonance Imaging–Assessed Atherosclerotic Plaque Burden.” Arteriosclerosis, thrombosis, and vascular biology (2020).
MLA
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Ben-Aicha, S., et al. “HDL (High-Density Lipoprotein) Remodeling and Magnetic Resonance Imaging–Assessed Atherosclerotic Plaque Burden.” Arteriosclerosis, Thrombosis, and Vascular Biology, 2020.
BibTeX Click to copy
@article{s2020a,
title = {HDL (High-Density Lipoprotein) Remodeling and Magnetic Resonance Imaging–Assessed Atherosclerotic Plaque Burden},
year = {2020},
journal = {Arteriosclerosis, thrombosis, and vascular biology},
author = {Ben-Aicha, S. and Casaní, L. and Muñoz-García, Natàlia and Joan-Babot, Oriol and Peña, E. and Aržanauskaitė, M. and Gutierrez, M. and Mendieta, G. and Padró, T. and Badimón, L. and Vilahur, G.}
}
Supplemental Digital Content is available in the text. Objective: HDL (high-density lipoprotein) role in atherosclerosis is controversial. Clinical trials with CETP (cholesterylester transfer protein)-inhibitors have not provided benefit. We have shown that HDL remodeling in hypercholesterolemia reduces HDL cardioprotective potential. We aimed to assess whether hypercholesterolemia affects HDL-induced atherosclerotic plaque regression. Approach and Results: Atherosclerosis was induced in New Zealand White rabbits for 3-months by combining a high-fat-diet and double-balloon aortic denudation. Then, animals underwent magnetic resonance imaging (basal plaque) and randomized to receive 4 IV infusions (1 infusion/wk) of HDL isolated from normocholesterolemic (NC-HDL; 75 mg/kg; n=10), hypercholesterolemic (HC-HDL; 75 mg/Kg; n=10), or vehicle (n=10) rabbits. Then, animals underwent a second magnetic resonance imaging (end plaque). Blood, aorta, and liver samples were obtained for analyses. Follow-up magnetic resonance imaging revealed that NC-HDL administration regressed atherosclerotic lesions by 4.3%, whereas, conversely, the administration of HC-HDLs induced a further 6.5% progression (P<0.05 versus basal). Plaque characterization showed that HC-HDL administered animals had a 2-fold higher lipid and cholesterol content versus those infused NC-HDL and vehicle (P<0.05). No differences were observed among groups in CD31 levels, nor in infiltrated macrophages or smooth muscle cells. Plaques from HC-HDL administered animals exhibited higher Casp3 (caspase 3) content (P<0.05 versus vehicle and NC-HDL) whereas plaques from NC-HDL infused animals showed lower expression of Casp3, Cox1 (cyclooxygenase 1), inducible nitric oxide synthase, and MMP (metalloproteinase) activity (P<0.05 versus HC-HDL and vehicle). HDLs isolated from animals administered HC-HDL displayed lower antioxidant potential and cholesterol efflux capacity as compared with HDLs isolated from NC-HDL-infused animal and vehicle or donor HDL (P<0.05). There were no differences in HDL-ApoA1 content, ABCA1 (ATP-binding cassette transporter A1) vascular expression, and SRB1 (scavenger receptor B1) and ABCA1 liver expression. Conclusions: HDL particles isolated from a hypercholesterolemic milieu lose their ability to regress and stabilize atherosclerotic lesions. Our data suggest that HDL remodeling in patients with co-morbidities may lead to the loss of HDL atheroprotective functions.
