HDL (High-Density Lipoprotein) Remodeling and Magnetic Resonance Imaging-Assessed Atherosclerotic Plaque Burden: Study in a Preclinical Experimental Model


Por: Ben-Aicha S., Casaní L., Muñoz-Garciá N., Joan-Babot O., Peña E., Aržanauskaite M., Gutierrez M., Mendieta G., Padró T., Badimon L., Vilahur G.

Publicada: 1 oct 2020 Ahead of Print: 1 ene 2020
Resumen:
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. © 2020 S. Karger AG. All rights reserved.

Filiaciones:
Ben-Aicha S.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

 School of Medicine, University of Barcelona (UB), Spain

Casaní L.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

Muñoz-Garciá N.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

Joan-Babot O.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

Peña E.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

 Centro de Investigación Biomédica en Red Cardiovascular (CIBERCV), Instituto de Salud Carlos III, Spain

Aržanauskaite M.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

Gutierrez M.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

 Cardiology Department, Hospital Clinico Barcelona Spain, Spain

Mendieta G.:
 School of Medicine, University of Barcelona (UB), Spain

Padró T.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

 Centro de Investigación Biomédica en Red Cardiovascular (CIBERCV), Instituto de Salud Carlos III, Spain

Badimon L.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

 Centro de Investigación Biomédica en Red Cardiovascular (CIBERCV), Instituto de Salud Carlos III, Spain

 Cardiovascular Research Chair, Universidad Autónoma Barcelona (UAB), Spain

Vilahur G.:
 Cardiovascular Program-ICCC, Research Institute-Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, Barcelona, Spain

 Centro de Investigación Biomédica en Red Cardiovascular (CIBERCV), Instituto de Salud Carlos III, Spain
ISSN: 10795642
Editorial
LIPPINCOTT WILLIAMS & WILKINS, TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 40 Número: 10
Páginas: 2481-2493
WOS Id: 000576399500016
ID de PubMed: 32847390
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