AIBP, Angiogenesis, Hematopoiesis, and Atherogenesis
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VASCULAR BIOLOGY (H. POWNALL, SECTION EDITOR)
AIBP, Angiogenesis, Hematopoiesis, and Atherogenesis Xueting Qiu 1 & Jingmin Luo 1 & Longhou Fang 1,2,3,4 Accepted: 11 November 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review The goal of this manuscript is to summarize the current understanding of the secreted APOA1 binding protein (AIBP), encoded by NAXE, in angiogenesis, hematopoiesis, and inflammation. The studies on AIBP illustrate a critical connection between lipid metabolism and the aforementioned endothelial and immune cell biology. Recent Findings AIBP dictates both developmental processes such as angiogenesis and hematopoiesis, and pathological events such as inflammation, tumorigenesis, and atherosclerosis. Summary Although cholesterol efflux dictates AIBP-mediated lipid raft disruption in many of the cell types, recent studies document cholesterol efflux-independent mechanism involving Cdc42-mediated cytoskeleton remodeling in macrophages. AIBP disrupts lipid rafts and impairs raft-associated VEGFR2 but facilitates non-raft–associated NOTCH1 signaling. Furthermore, AIBP can induce cholesterol biosynthesis gene SREBP2 activation, which in turn transactivates NOTCH1 and supports specification of hematopoietic stem and progenitor cells (HSPCs). In addition, AIBP also binds TLR4 and represses TLR4-mediated inflammation. In this review, we summarize the latest research on AIBP, focusing on its role in cholesterol metabolism and the attendant effects on lipid raft–regulated VEGFR2 and non-raft–associated NOTCH1 activation in angiogenesis, SREBP2-upregulated NOTCH1 signaling in hematopoiesis, and TLR4 signaling in inflammation and atherogenesis. We will discuss its potential therapeutic applications in angiogenesis and inflammation due to selective targeting of activated cells. Keywords AIBP . Cholesterol efflux . SREBP2-regulated Notch . Angiogenesis and hematopoiesis . TLR4 signaling . Atherogenesis
Introduction Xueting Qiu and Jingmin Luo contributed equally to this work. This article is part of the Topical Collection on Vascular Biology * Longhou Fang [email protected] Xueting Qiu [email protected] Jingmin Luo [email protected] 1
Center for Cardiovascular Regeneration, Department of Cardiovascular Sciences, Houston Methodist Research Institute, 6550 Fannin Street, Houston, TX 77030, USA
2
Department of Obstetrics and Gynecology, Houston Methodist Research Institute, 6550 Fannin Street, Houston, TX 77030, USA
3
Houston Methodist Institute for Academic Medicine, Houston Methodist Research Institute, 6550 Fannin Street, Houston, TX 77030, USA
4
Department of Cardiothoracic Surgeries, Weill Cornell Medical College, Cornell University, New York, NY 10065, USA
Cholesterol is the fundamental building block of the cell, but it is also toxic to the cell if accumulated in excess. Maintenance of cellular cholesterol homeostasis is therefore essential for normal cell function [1–6]. As such, the cell has evolved a delicate program t
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