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ApoB-containing lipoproteins regulate angiogenesis by modulating expression of VEGF receptor 1. 2012
Inbal Avraham-Davidi, and
Yona Ely, and
Van N Pham, and
Daniel Castranova, and
Moshe Grunspan, and
Guy Malkinson, and
Liron Gibbs-Bar, and
Oded Mayseless, and
Gabriella Allmog, and
Brigid Lo, and
Carmen M Warren, and
Tom T Chen, and
Josette Ungos, and
Kameha Kidd, and
Kenna Shaw, and
Ilana Rogachev, and
Wuzhou Wan, and
Philip M Murphy, and
Steven A Farber, and
Liran Carmel, and
Gregory S Shelness, and
M Luisa Iruela-Arispe, and
Brant M Weinstein, and
Karina Yaniv
Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.
Despite the clear major contribution of hyperlipidemia to the prevalence of cardiovascular disease in the developed world, the direct effects of lipoproteins on endothelial cells have remained obscure and are under debate. Here we report a previously uncharacterized mechanism of vessel growth modulation by lipoprotein availability. Using a genetic screen for vascular defects in zebrafish, we initially identified a mutation, stalactite (stl), in the gene encoding microsomal triglyceride transfer protein (mtp), which is involved in the biosynthesis of apolipoprotein B (ApoB)-containing lipoproteins. By manipulating lipoprotein concentrations in zebrafish, we found that ApoB negatively regulates angiogenesis and that it is the ApoB protein particle, rather than lipid moieties within ApoB-containing lipoproteins, that is primarily responsible for this effect. Mechanistically, we identified downregulation of vascular endothelial growth factor receptor 1 (VEGFR1), which acts as a decoy receptor for VEGF, as a key mediator of the endothelial response to lipoproteins, and we observed VEGFR1 downregulation in hyperlipidemic mice. These findings may open new avenues for the treatment of lipoprotein-related vascular disorders.
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