Apolipoprotein A-1 binding protein promotes macrophage cholesterol efflux by facilitating apolipoprotein A-1 binding to ABCA1 and preventing ABCA1 degradation

Zhang, Min; Liang, Li; Xie, Wei; Wu, Jianfeng; Yao, Feng; Tan, Yanhong; Xia, Xiao-Dan; Liu, Xiaoyan; Liu, Dan; Lan, Gang; Zeng, Meng-Ya; Gong, Duo; Cheng, Haipeng; Huang, Chong; Zhao, Zhen-Wang; Zheng, Xi-Long; Tang, Chao-Ke

doi:10.1016/j.atherosclerosis.2016.03.008

Cited by 72 publications

(39 citation statements)

References 40 publications

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“…2C). In these and further experiments, we used a dose of AIBP (0.2 μg/ml) previously selected in experiments with endothelial cells and macrophages (Fang et al, 2013; Zhang et al, 2016). …”

Section: Resultsmentioning

confidence: 99%

“…Human APOA1BP mRNA is ubiquitously expressed and the AIBP protein is found in cerebrospinal fluid (CSF) and urine (Ritter et al, 2002) and can be detected in plasma. AIBP has been shown to bind ApoA-I and HDL (Fang et al, 2013; Ritter et al, 2002) and augment cholesterol efflux from endothelial cells and macrophages (Fang et al, 2013; Zhang et al, 2016). Cholesterol efflux regulates the abundance and integrity of lipid rafts, plasma membrane microdomains characterized by a high content of cholesterol and sphingolipids, which serve as functional platforms for the regulation of many surface receptors (Sezgin et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States

et al. 2018

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SUMMARY Apolipoprotein A-I binding protein (AIBP) reduces lipid raft abundance by augmenting removal of excess of cholesterol from the plasma membrane. Here, we report that AIBP prevents and reverses processes associated with neuroinflammatory-mediated spinal nociceptive processing. The mechanism involves AIBP binding to Toll-like-receptor-4 (TLR4) and increased binding of AIBP to activated microglia, which mediates selective regulation of lipid rafts in inflammatory cells. AIBP-mediated lipid raft reductions downregulated LPS-induced TLR4 dimerization, inflammatory signaling and expression of cytokines in microglia. In mice, intrathecal injections of AIBP reduced spinal myeloid cell lipid rafts, TLR4 dimerization, neuroinflammation, and glial activation. Intrathecal AIBP reversed established allodynia in mice in which pain states were induced by the chemotherapeutic cisplatin, intraplantar formalin, or intrathecal LPS, all pro-nociceptive interventions known to be regulated by TLR4 signaling. These findings demonstrate a mechanism by which AIBP regulates neuroinflammation and suggest the therapeutic potential for AIBP in treating preexisting pain states.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States

et al. 2018

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“…ABCA1 is expressed in various tissues and organs, and the function of ABCA1 is not similar in different organ tissues . The decrease in ABCA1 expression in the local part of the vessel wall is related to the deposition of lipid in the vessel wall and the vascularization of atherosclerosis . The expression at the fork or bend is significantly lower than the vertical.…”

Section: Discussionmentioning

confidence: 99%

ABCA1 variants rs2230806 (R219K), rs4149313 (M8831I), and rs9282541 (R230C) are associated with susceptibility to coronary heart disease

Wang

Chen

et al. 2019

Clinical Laboratory Analysis

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BackgroundTo investigate the association between three single nucleotide polymorphisms (SNPs) of ABCA1 gene and susceptibility to coronary heart disease (CHD) in Chinese Han population.MethodsA total of 484 CHD patients and 488 controls were included in the study. Three SNPs rs2230806 (R219K), rs4149313 (M8831I), and rs9282541 (R230C) in ABCA1 gene were genotyped by SNaPshot.ResultsSingle nucleotide polymorphism rs1800977 was associated with susceptibility to CHD (AA vs GG, P = 0.013; A vs G, P = 0.029; recessive model, P = 0.020). Rs4149313 (AA vs GG, P = 0.010; recessive model, P = 0.011) and rs9282541 (T vs C, P = 0.029; dominant model, P = 0.039) were also risk factor for CHD.ConclusionThis study suggests that three SNPs rs2230806, rs4149313, and rs9282541 in ABCA1 gene are significantly associated with susceptibility to CHD; further mechanism should be performed to be applied to drug research and development.

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“…Mechanistically, AIBP accelerates cholesterol efflux from ECs to HDL, which in turn reduces the amount of plasma membrane cholesterol available for lipid raft formation, thereby impairing VEGFR2 signaling competence 27 . Extracellular AIBP promotes cholesterol efflux from human macrophages, thereby reducing lipid accretion 28 . AIBP, encoded by the Apoa1bp gene in mice and APOA1BP gene in humans, is a secreted protein that physically associates with apoA-I 29 ; AIBP is ubiquitously expressed and abundant in most human organs with secretory functions.…”

Section: Introductionmentioning

confidence: 99%

AIBP Limits Angiogenesis Through γ-Secretase-Mediated Upregulation of Notch Signaling

Mao

Meng

et al. 2017

Circulation Research

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Rationale Angiogenesis improves perfusion to the ischemic tissue following acute vascular obstruction. Angiogenesis in pathophysiological settings reactivates signaling pathways involved in developmental angiogenesis. We showed previously that apoA-I binding protein (AIBP)-regulated cholesterol efflux in endothelial cells (ECs) controls zebrafish embryonic angiogenesis. Objective This study is to determine whether loss of AIBP affects angiogenesis in mice during development and under pathological conditions, and to explore the underlying molecular mechanism. Methods and Results In this paper, we report the generation of AIBP knockout (Apoa1bp−/−) mice, which are characterized of accelerated postnatal retinal angiogenesis. Mechanistically, AIBP triggered relocalization of γ-secretase from lipid rafts to non-lipid rafts where it cleaved Notch. Consistently, AIBP treatment enhanced DLL4-stimulated Notch activation in human retinal ECs. Increasing HDL levels in Apoa1bp−/− mice by crossing them with apoA-I transgenic mice rescued Notch activation and corrected dysregulated retinal angiogenesis. Notably, the retinal vessels in Apoa1bp−/− mice manifested normal pericyte coverage and vascular integrity. Similarly, in the subcutaneous Matrigel plug assay, which mimics ischemic/inflammatory neovascularization, angiogenesis was dramatically upregulated in Apoa1bp−/− mice and associated with a profound inhibition of Notch activation and reduced expression of downstream targets. Furthermore, loss of AIBP increased vascular density and facilitated the recovery of blood vessel perfusion function in a murine hindlimb ischemia model. In addition, AIBP expression was significantly increased in human patients with ischemic cardiomyopathy. Conclusions Our data reveal a novel mechanistic connection between AIBP-mediated cholesterol metabolism and Notch signaling, implicating AIBP as a possible druggable target to modulate angiogenesis under pathological conditions.

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Apolipoprotein A-1 binding protein promotes macrophage cholesterol efflux by facilitating apolipoprotein A-1 binding to ABCA1 and preventing ABCA1 degradation

Cited by 72 publications

References 40 publications

Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States

Inhibition of Neuroinflammation by AIBP: Spinal Effects upon Facilitated Pain States

ABCA1 variants rs2230806 (R219K), rs4149313 (M8831I), and rs9282541 (R230C) are associated with susceptibility to coronary heart disease

AIBP Limits Angiogenesis Through γ-Secretase-Mediated Upregulation of Notch Signaling

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