Role of the ABC transporters A1 and G1, key reverse cholesterol transport proteins, in atherosclerosis

Demina, E. P.; Miroshnikova, V. V.; Schwarzman, A. L.

doi:10.1134/s0026893316020047

Cited by 29 publications

(17 citation statements)

References 47 publications

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“…TD is caused by loss-of-function (LOF) mutations in the ATP-binding cassette transporter A1 ( ABCA1 ) gene (1–3), encoding the membrane transporter ABCA1. This transporter plays an important role in the efflux of free cholesterol (FC) from peripheral cells and its transfer to lipid-poor Apo A-I particles, which represents the first stage of reverse cholesterol transport (RCT) pathway (4–8). Therefore, ABCA1 deficiency leads to intracellular accumulation of CE, precludes the conversion of the lipid-poor Apo A-I particles into pre-β HDL, and promotes a rapid catabolism of the poorly lipidated Apo A-I, mostly by the kidney (9).…”

Section: Introductionmentioning

confidence: 99%

A Novel Mutation in ABCA1 Gene Causing Tangier Disease in an Italian Family with Uncommon Neurological Presentation

et al. 2016

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Tangier disease is an autosomal recessive disorder characterized by severe reduction in high-density lipoprotein cholesterol and peripheral lipid storage. We describe a family with c.5094C > A p.Tyr1698* mutation in the ABCA1 gene, clinically characterized by syringomyelic-like anesthesia, demyelinating multineuropathy, and reduction in intraepidermal small fibers innervation. In the proband patient, cardiac involvement determined a myocardial infarction; lipid storage was demonstrated in gut, cornea, and aortic wall. The reported ABCA1 mutation has never been described before in a Tangier family.

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Section: Introductionmentioning

confidence: 99%

A Novel Mutation in ABCA1 Gene Causing Tangier Disease in an Italian Family with Uncommon Neurological Presentation

et al. 2016

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“…A growing body of evidence suggests that high density lipoprotein (HDL) plays an important role in the removal of cholesterol from atherosclerotic plaques and the transport of excess cholesterol back to the liver, and this is one of the main mechanisms to prevent the occurrence of AS, which called reverse cholesterol transport (RCT) [7][8][9]. ATP binding cassettes (ABC) A1 and G1 are key genes in RCT process [10,11]. ABCA1 has been reported to play an important role in the prevention of AS by facilitating cholesterol efflux and decreasing cholesterol accumulation in macrophages [10,12].…”

Section: Introductionmentioning

confidence: 99%

Recombinant Klotho protein enhances cholesterol efflux of THP-1 macrophage-derived foam cells via suppressing Wnt/β-catenin signaling pathway

Liu

Chen

et al. 2020

BMC Cardiovasc Disord

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Background: Atherosclerosis (AS) is the basis of cardiovascular diseases, characterized by chronic inflammatory and lipid metabolism disorders. Although the anti-inflammatory effect of Klotho in AS has been clearly shown, its lipidlowering effect is unclear. In this study, we examined the effects of recombinant Klotho (Re-KL) protein on lipid accumulation in foam cells. Methods: THP-1 cells were exposed to 100 nM phorbol myristate acetate for 24 h and then to oxidized low-density lipoprotein (ox-LDL; 80 mg/mL) to induce foam cell formation. Subsequently, the foam cells were incubated with Re-KL and/or DKK1, an inhibitor of the Wnt/β-catenin pathway. Results: Oil red O staining and cholesterol intake assay revealed that the foam cell model was constructed successfully. Pretreatment of the foam cells with Re-KL decreased total cholesterol level, up-regulated the expression of ATP binding cassette transporter A1 (ABCA1) and G1 (ABCG1), and down-regulated the expression of acyl coenzyme a-cholesterol acyltransferase 1 (ACAT1) and members of the scavenger family (SR-A1 and CD36). In addition, the expression of Wnt/β-catenin pathwayrelated proteins in foam cells was significantly decreased by the stimulus of Re-KL. Interestingly, the effect of Re-KL was similar to that of DKK1 on foam cells. Conclusions: The Re-KL-induced up-regulation of reverse cholesterol transport capacity promotes cholesterol efflux and reduces lipid accumulation by suppressing the Wnt/β-catenin pathway in foam cells.

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“…ABCG1 has a critical role in mediating cholesterol efflux to HDL and preventing cellular lipid accumulation [12][13][14]. ABCA1 and ABCG1 can be highly induced in macrophages [15]. It was found that the expression of ABCA1 is mainly regulated by nuclear receptors LXRα and LXRβ, while LXRα is regulated by PPARc [16,17].…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Shenqi Maixintong Capsule against ox‐LDL‐Induced Injury in RAW264.7 Macrophages

Liang

Cai

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Shenqi Maixintong capsule (SMC), a traditional Chinese medicine compound, exerts various therapeutic effects, including nourishing one’s vitality, improving blood circulation, regulating vital energy, and promoting coronary circulation. Studies have demonstrated that SMC could effectively alleviate atherosclerosis (AS) and delay its development. However, the effect of SMC on lipid metabolism remains unclear. Herein, we investigated the mechanism of SMC on lipid metabolism of RAW264.7 cells induced by oxidized low-density lipoprotein (ox-LDL). Drug-containing serum was prepared by intragastric administration of SD (Sprague Dawley) rats. RAW264.7 cells were transformed into foam cells with 25 mg/L ox-LDL. SMC-treated rat serum increased the survival rate of ox-LDL-induced RAW264.7 cells. Oil Red staining, total cholesterol, and free cholesterol detection data showed that the intermediated dose of SMC had the best effect on reducing the lipid accumulation, lipid droplets, intracellular cholesterol, and total cholesterol content of RAW264.7 cells. The results of western blotting showed that the expression of ABCA1, ABCG1, LXRα, PPARγ, and peroxisome proliferation-activated receptor alpha (PPARα) was increased by SMC, and proprotein convertase subtilisin/kexin type 9 (PCSK9) was reduced, which promoted reverse cholesterol transport (RCT) of RAW264.7 cells and inhibited foam cell formation. Furthermore, SOD and MDA data indicated that SMC could reduce the senescence of RAW264.7 cells. These findings suggest that SMC might prevent ox-LDL-induced damage of macrophages in AS patients by improving cell viability and slowing down lipid accumulation and senescence.

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Role of the ABC transporters A1 and G1, key reverse cholesterol transport proteins, in atherosclerosis

Cited by 29 publications

References 47 publications

A Novel Mutation in ABCA1 Gene Causing Tangier Disease in an Italian Family with Uncommon Neurological Presentation

A Novel Mutation in ABCA1 Gene Causing Tangier Disease in an Italian Family with Uncommon Neurological Presentation

Recombinant Klotho protein enhances cholesterol efflux of THP-1 macrophage-derived foam cells via suppressing Wnt/β-catenin signaling pathway

Protective Effect of Shenqi Maixintong Capsule against ox‐LDL‐Induced Injury in RAW264.7 Macrophages

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