Effect of Apolipoprotein A-I on ATP Binding Cassette Transporter A1 Degradation and Cholesterol Efflux in THP-1 Macrophage-derived Foam Cells

Tang, Chao-Ke; Tang, Guoyao; Yi, Guanghui; Zuo, Wang; Liu, Lu‐Shan; Wan, Shuang; Yuan, Zhonghua; He, Xiu‐Sheng; Yang, Jun-Hao; Ruan, Changgeng; Yong, Yang

doi:10.1093/abbs/36.3.218

Cited by 34 publications

(19 citation statements)

References 27 publications

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“…Moreover, we also discovered that oleic acid might decrease ABC-A1 expression. Furthermore, 22-R-hydroxycholesterol stimulates ABC-A1 expression and cholesterol efflux in THP-1-derived foam cells [36] . These experimental data suggest that ABC-A1 may mediate cholesterol exchanges between the cellular membrane and HDL.…”

Section: Transmembrane Transport System Of the Abc-a1 Complexmentioning

confidence: 96%

A novel model of cholesterol efflux from lipid-loaded cells

et al. 2010

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Cholesterol efflux from lipid-loaded cells is a key athero-protective event that counteracts cholesterol uptake. The imbalance between cholesterol efflux and uptake determines the prevention or development of atherosclerosis. Many proteins and factors participate in the cholesterol efflux event. However, there are currently no systematic models of reverse cholesterol transport (RCT) that include most RCT-related factors and events. On the basis of recent research findings from other and our laboratories, we propose a novel model of one center and four systems with coupling transportation and networking regulation. This model represents a common way of cholesterol efflux; however, the systems in the model consist of different proteins/factors in different cells. In this review, we evaluate the novel model in vascular smooth muscle cells (VSMCs) and macrophages, which are the most important original cells of foam cells. This novel model consists of 1) a caveolae transport center, 2) an intracellular trafficking system of the caveolin-1 complex, 3) a transmembrane transport system of the ABC-A1 complex, 4) a transmembrane transport system of the SR-B1 complex, and 5) an extracelluar trafficking system of HDL/Apo-A1. In brief, the caveolin-1 system transports cholesterol from intracellular compartments to caveolae. Subsequently, both ABC-A1 and SR-B1 complex systems transfer cholesterol from caveolae to extracellular HDL/Apo-A1. The four systems are linked by a regulatory network. This model provides a simple and concise way to understand the dynamic process of atherosclerosis.

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Section: Transmembrane Transport System Of the Abc-a1 Complexmentioning

confidence: 96%

A novel model of cholesterol efflux from lipid-loaded cells

et al. 2010

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“…Although apoA-I does not alter ABCA1 mRNA abundance, it increases the content of ABCA1 protein markedly, suggesting the effect of apoA-I on ABCA1 degradation (35). Studies have shown several possible mechanisms that contribute to ABCA1 protein stabilization; for example, interactions of ABCA1 and apoA-I interfered with the phosphorylation of the PEST sequence and reduced calpain-mediated proteolysis (10,(36)(37)(38).…”

Section: The Reciprocal Response Of the Binding Of Apoa-i/abca1mentioning

confidence: 99%

The Interaction of ApoA-I and ABCA1 Triggers Signal Transduction Pathways to Mediate Efflux of Cellular Lipids

Zhao

Yin

et al. 2011

Mol Med

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Reverse cholesterol transport (RCT) has been characterized as a crucial step for antiatherosclerosis, which is initiated by ATPbinding cassette A1 (ABCA1) to mediate the efflux of cellular phospholipids and cholesterol to lipid-free apolipoprotein A-I (apoA-I). However, the mechanisms underlying apoA-I/ABCA1 interaction to lead to the lipidation of apoA-I are poorly understood. There are several models proposed for the interaction of apoA-I with ABCA1 as well as the lipidation of apoA-I mediated by ABCA1. ApoA-I increases the levels of ABCA1 protein markedly. In turn, ABCA1 can stabilize apoA-I. The interaction of apoA-I with ABCA1 could activate signaling molecules that modulate posttranslational ABCA1 activity or lipid transport activity. The key signaling molecules in these processes include protein kinase A (PKA), protein kinase C (PKC), Janus kinase 2 (JAK2), Rho GTPases and Ca 2+ , and many factors also could influence the interaction of apoA-I with ABCA1. This review will summarize these mechanisms for the apoA-I interaction with ABCA1 as well as the signal transduction pathways involved in these processes.

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“…Our previous studies demonstrated that ox-LDL 20) , thiol protease inhibitors 21) , and NO-1886 22) elevated ABCA1 expression. Oleate 23) , eicosapentaenoic acid 24) and IFN-gamma 25) reduced the level of ABCA1 and impaired ABCA1-dependent cholesterol efflux in THP-1 macrophage-derived foam cells.…”

Section: Introductionmentioning

confidence: 92%

“…Oleate 23) , eicosapentaenoic acid 24) and IFN-gamma 25) reduced the level of ABCA1 and impaired ABCA1-dependent cholesterol efflux in THP-1 macrophage-derived foam cells. LXR agonist promoted ABCA1 expression in apoE KO mice 26) .…”

Section: Introductionmentioning

confidence: 94%