Abstract Or132: The N-terminus of Apolipoprotein B mediates the interaction of atherogenic lipoproteins with endothelial cells

Apolipoprotein B (APOB) containing lipoproteins contribute to atherosclerosis by entering the arterial wall through the endothelial cell surface receptors scavenger receptor-BI (SR-BI) and activin receptor-like kinase 1 (ALK1). We used N-terminal fragments of APOB, molecular modeling, and site-directed mutagenesis to identify and block the binding of chylomicrons and LDL to these receptors in cells and mice. We discovered that different regions interact with SR-BI and ALK1. A fragment of APOB, comprising 18% of the N-terminal sequence (APOB18), reduced the uptake and transport of both chylomicrons and LDL by endothelial cells. Importantly, overexpressing APOB18 decreased atherosclerosis in hypercholesterolemic mice. These findings identify the N-terminal region of APOB as the cause of atherosclerosis and illustrate an approach to treating or preventing vascular disease

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Journal
Arteriosclerosis Thrombosis and Vascular Biology
Published
2025-04-01
DOI
https://doi.org/10.1161/atv.45.suppl_1.or132
Primary Topic
Lipoproteins and Cardiovascular Health
Type
article
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article

Abstract Or132: The N-terminus of Apolipoprotein B mediates the interaction of atherogenic lipoproteins with endothelial cells

Swati Valmiki, Jenny E. Kanter, Narasimha Anaganti, Karin Bornfeldt et al.
Arteriosclerosis Thrombosis and Vascular Biology
Lipoproteins and Cardiovascular Health
article

Abstract Or132: The N-terminus of Apolipoprotein B mediates the interaction of atherogenic lipoproteins with endothelial cells

Swati Valmiki, Jenny E. Kanter, Narasimha Anaganti, Karin Bornfeldt, Jana Gjini, Nicholas O. Davidson, M. Mahmood Hussain, Dimitrios Nasias, Tobias Madl, Ira J. Goldberg, Waqas Younis, Tse Wing Winnie Ho, Edward A. Fisher, Warren Lee, Carmen Nikain, Rufina Kore, Ainara González
article en

Abstract

Apolipoprotein B (APOB) containing lipoproteins contribute to atherosclerosis by entering the arterial wall through the endothelial cell surface receptors scavenger receptor-BI (SR-BI) and activin receptor-like kinase 1 (ALK1). We used N-terminal fragments of APOB, molecular modeling, and site-directed mutagenesis to identify and block the binding of chylomicrons and LDL to these receptors in cells and mice. We discovered that different regions interact with SR-BI and ALK1. A fragment of APOB, comprising 18% of the N-terminal sequence (APOB18), reduced the uptake and transport of both chylomicrons and LDL by endothelial cells. Importantly, overexpressing APOB18 decreased atherosclerosis in hypercholesterolemic mice. These findings identify the N-terminal region of APOB as the cause of atherosclerosis and illustrate an approach to treating or preventing vascular disease

Arteriosclerosis Thrombosis and Vascular BiologyVol. 45(Suppl_1)
Long Island University (US), University of Graz (AT), Homi Bhabha National Institute (IN), University of Washington (US), Washington University in St. Louis (US), NYU Langone Health (US), New York University (US)
Good health and well-being
Openalex Percentile: Top 75%
Lipoproteins and Cardiovascular Health
DOISourceOpenAlex
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