A5015372221- Atherosclerosis and Cardiovascular Diseases
- Adipokines, Inflammation, and Metabolic Diseases
- Antioxidant Activity and Oxidative Stress
- Protease and Inhibitor Mechanisms
- Galectins and Cancer Biology
- Cell Adhesion Molecules Research
- Seaweed-derived Bioactive Compounds
- Monoclonal and Polyclonal Antibodies Research
- Lipoproteins and Cardiovascular Health
- Systemic Lupus Erythematosus Research
- Chemokine receptors and signaling
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cardiovascular Disease and Adiposity
- Cancer, Lipids, and Metabolism
- Protein Tyrosine Phosphatases
- Immune cells in cancer
- Single-cell and spatial transcriptomics
- Apelin-related biomedical research
- Peroxisome Proliferator-Activated Receptors
- Cardiac Health and Mental Health
- Immune Response and Inflammation
- Free Radicals and Antioxidants
- Viral Infectious Diseases and Gene Expression in Insects
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Diabetes, Cardiovascular Risks, and Lipoproteins
Center of Molecular Immunology (Cuba)
2013-2024
University of Alberta
2018-2024
Université de Montréal
2012-2020
Alberta Hospital Edmonton
2016
Centro de Ingeniería Genética y Biotecnología
2012
University of Havana
2012
Applied Scientific Research (United States)
2012
Atherosclerosis is triggered by the retention of apolipoprotein B-containing lipoproteins proteoglycans. In addition to low-density lipoprotein, remnant have emerged as pivotal contributors this pathology, particularly in context insulin resistance and diabetes. We previously reported antiatherogenic properties a monoclonal antibody (chP3R99) that recognizes sulfated glycosaminoglycans on arterial
Subendothelial retention of proatherogenic lipoproteins by proteoglycans is critical in atherosclerosis. The aim this study was to characterize the recognition and antiatherogenic properties a chimeric monoclonal antibody (mAb) that reacts with sulfated molecules.chP3R99 mAb recognized glycosaminoglycans, mainly chondroitin sulfate (CS), ELISA. This blocked ≈70% low-density lipoprotein (LDL)-CS association ≈80% LDL oxidation vitro, when intravenously injected Sprague-Dawley rats (n=6, 1...
Objective— The pathogenesis of atherosclerosis is associated with the early retention low-density lipoproteins that are trapped in extracellular matrix arterial intima by interaction glycosaminoglycan side chains proteoglycans. Mutant mouse/human chimeric antibodies murine monoclonal antibody P3, which react N-glycolyl–containing gangliosides and sulfated glycosaminoglycans, were tested for their potentially antiatherogenic properties through induction an idiotypic network may specifically...
Atherosclerosis represents a major cause of death in the world. It is known that Lipofundin 20% induces atherosclerotic lesions rabbits, but its effects on serum lipids behaviour and redox environment have not been addressed. In this study, New Zealand rabbits were treated with 2 mL/kg for 8 days. Then, biomarkers determined spectrophotometrically. On other hand, development was confirmed by eosin/hematoxylin staining electron microscopy. At end experiment, total cholesterol, triglycerides,...
The relationship between autoantibodies (autoAbs) to oxidized LDL (oxLDL) and coronary artery disease (CAD) remains controversial. IgM IgG autoAbs oxLDL 1-palmitoyl-2 (5'-oxo-valeroyl)-sn-glycero-3-phosphorylcholine (POVPC), as well the levels of non modified or ApoB-100 immune complexes (ICs), were measured in twenty patients undergoing clinically indicated angiography, ten young healthy volunteer sera. did not differ no CAD subjects, but these significantly higher subjects comparison with...
Retained low-density lipoproteins (LDL) by arterial glycosaminoglycans (GAG) are more susceptible to reactive oxygen species-mediated oxidation, contributing oxidative stress and atherosclerosis. Recently, we reported the properties of chimeric mouse/human monoclonal antibody chP3R99-LALA bind sulfated GAG, inhibit LDL-chondroitin sulfate binding, avoid LDL oxidation in vitro. Here, hypothesized that treatment might reduce aortic a therapeutic setting. Redox biomarkers serum lipids were...
The progression of atherosclerosis is favored by increasing amounts chondroitin sulfate proteoglycans in the artery wall. We previously reported reactivity chP3R99 monoclonal antibody (mAb) with sulfated glycosaminoglycans and its association anti-atherogenic properties displayed. Now, we evaluated accumulation this mAb atherosclerotic lesions potential use as a probe for specific vivo detection disease. Atherosclerosis was induced NZW rabbits (n = 14) administration Lipofundin 20% using...
LDL oxidation and oxidative stress are closely related to atherosclerosis. Therefore, natural antioxidants have been studied as promising candidates. In the present study, inhibition activity of bioactive compounds from Halimeda incrassata seaweed. associated antioxidant capacity, was evaluated in vitro. Experimental work conducted with lyophilized aqueous extract phenolic-rich fractions seaweed their effect on using heparin-precipitated (hep-LDL) exposure Cu2+ ions AAPH free radical...
Atherosclerosis, the underlying pathology of most cardiovascular diseases, is triggered by retention apolipoprotein B (apoB)-containing lipoproteins in arterial wall through electrostatic interactions with glycosaminoglycan (GAG) side chains proteoglycans. Previously, we reported antiatherogenic properties chimeric monoclonal antibody (mAb) chP3R99-LALA, which binds sulfated GAGs, inhibits low-density lipoprotein (LDL)-chondroitin sulfate (CS) association, and abrogates LDL oxidation foam...
The retention of lipoprotein particles in the intima, particular to glycosaminoglycan side chains proteoglycans, is a critical step atherosclerosis initiation. Administration chP3R99, chimeric mouse/human monoclonal antibody inducing an anti-idiotypic network response against glycosaminoglycans was previously shown prevent atherosclerotic lesion progression, yet its effect late-stage progression lesions remains unknown. This study investigated chP3R99 at late stage disease development...
Background and aimsScavenger receptor class B member 3, also known as cluster of differentiation-36 (CD36) receptor, is involved in the uptake accumulation modified lipoprotein macrophages, driving atherosclerosis progression. Azapeptide analogs growth hormone-releasing peptide-6 (GHRP-6) have been developed selective CD36 ligands evaluated for their anti-atherosclerotic properties apoe−/− mice.MethodsFrom 4 to 19 weeks age, male mice were fed a high fat cholesterol (HFHC) diet, then...
ABSTRACT Atherosclerosis is initiated by the retention of ApoB-containing lipoproteins in arterial wall, mediated glycosaminoglycan chains proteoglycans. At Center for Molecular Immunology, we are developing P3R99 monoclonal antibody (mAb) to target this process. This study characterizes new mAb variants expressed CHO-K1 and HEK-293 cell lines. We compared these with parental from NS0 cells using SDS-PAGE, size exclusion cation exchange chromatography, dynamic light scattering, peptide...
Background: The response-to-retention hypothesis for atherosclerosis describes subendothelial retention of apolipoprotein B-containing lipoproteins mediated by proteoglycans (PG). Further we know that diabetes is also associated with both increased circulating chylomicron remnants and remodeling proatherogenic PGs. We have recently reported antiatherogenic properties a novel chimeric monoclonal antibody (chP3R99) recognizes PG sulfated molecules. Hypothesis: chP3R99 may interfere the...
Subendothelial retention of apoB-containing lipoproteins by interaction with glycosaminoglycan-side chains proteoglycans is considered the key initiating step atherogenesis. Previously, we characterized antiatherogenic properties chimeric mAb chP3R99, which binds sulfated GAG, inhibits LDL-chondroitin sulfate (CS) association, and abrogates LDL oxidation in vitro vivo. In preventive settings, rabbits mice immunized this showed reduced atherosclerotic lesions, related induction...
Aim: The aim of this work was to evaluate the in vitro atheroprotective potential seaweed Halimeda incrassata smooth muscle cell migration and lipoprotein oxidation relation its antioxidant activity.Material methods: Antioxidant activity determinate by DPPH• radical scavenging assay ORAC method. inhibitory effect aqueous extract on LDL mediated Cu2+ ions TBARS conjugated diene quantification. evaluated MOVAS-1 mouse aortic cell.Results: demonstrated. Seaweed caused dose-dependent inhibition...