Adiponectin prevents atherosclerosis by increasing cholesterol efflux from macrophages

Tsubakio-Yamamoto, Kazumi; Matsuura, Fumihiko; Koseki, Masahiro; Oku, Hiroyuki; Sandoval, Jose C.; Inagaki, Miwako; Nakatani, Kazuhiro; Nakaoka, Hajime; Kawase, Ryota; Yuasa-Kawase, Miyako; Masuda, Daisuke; Ohama, Tohru; Maeda, Norikazu; Nakagawa-Toyama, Yumiko; Ishigami, Masato; Nishida, Makoto; Kihara, Shinji; Shimomura, Iichiro; Yamashita, Shizuya

doi:10.1016/j.bbrc.2008.08.009

Cited by 113 publications

(72 citation statements)

References 14 publications

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“…Furthermore, we also found that the reduction of ABCA1 in overweight and obese patients was related to lower circulating level of the antiatherogenic adipokine adiponectin, but not associated with higher levels of the proatherogenic adipokines leptin and resistin. This is in keeping with data from in vitro experiments and animal studies showing that adiponectin can upregulate ABCA1 expression and cholesterol efflux from macrophages, [11][12] and knockout adiponectin can decrease the expression of ABCA1. 12 The activation of peroxisome proliferator-activated receptor g (PPARg) and liver X receptor a (LXRa) is the major mechanism through which macrophage ABCA1 and ABCG1 expression can be upregulated.…”

Section: Abca1 Expression In Obesitysupporting

confidence: 88%

“…This is in keeping with data from in vitro experiments and animal studies showing that adiponectin can upregulate ABCA1 expression and cholesterol efflux from macrophages, [11][12] and knockout adiponectin can decrease the expression of ABCA1. 12 The activation of peroxisome proliferator-activated receptor g (PPARg) and liver X receptor a (LXRa) is the major mechanism through which macrophage ABCA1 and ABCG1 expression can be upregulated. 2 In vitro experiments and animal studies have suggested that adiponectin can increase apoAI-mediated cholesterol efflux from macrophages through ABCA1-dependent pathway by the activation of PPARg and LXRa.…”

Section: Abca1 Expression In Obesitysupporting

confidence: 88%

“…2 In vitro experiments and animal studies have suggested that adiponectin can increase apoAI-mediated cholesterol efflux from macrophages through ABCA1-dependent pathway by the activation of PPARg and LXRa. 12 Our present study has added in vivo evidence that ABCA1 expression in overweight and obese patients is altered and it is related to the reduction of adiponectin. Whether the in vivo modulation of ABCA1 by adiponectin in our patients may be through the similar mechanism of PPARg/LXRa pathway remains to be confirmed.…”

Section: Abca1 Expression In Obesitymentioning

confidence: 58%

“…[9][10] Concerning macrophage RCT, in vitro experiments have shown that adiponectin can upregulate the expression of ABCA1 and cholesterol efflux from human macrophages. [11][12] In adiponectin knockout mice, the expression of ABCA1 and cholesterol efflux from macrophages is decreased compared with wild-type mice. 12 However, whether adiponectin may influence ABCG1 and SR-BI is unclear, and few studies about the effects of adiponectin on cholesterol efflux from macrophages in humans have been carried out.…”

Section: Introductionmentioning

confidence: 99%

“…[11][12] In adiponectin knockout mice, the expression of ABCA1 and cholesterol efflux from macrophages is decreased compared with wild-type mice. 12 However, whether adiponectin may influence ABCG1 and SR-BI is unclear, and few studies about the effects of adiponectin on cholesterol efflux from macrophages in humans have been carried out.…”

Section: Introductionmentioning

confidence: 99%

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The expression of ATP-binding cassette transporter A1 in Chinese overweight and obese patients

Zhou

Wang

et al. 2009

Int J Obes

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Background: ATP-binding cassette transporters (ABCA1, ABCG1) and scavenger receptor class B type I (SR-BI) are the three most important cellular cholesterol transporters/receptor in regulating cholesterol efflux. We have investigated whether the expression of these transporters/receptor is altered in overweight and obese patients, and the potential association with the circulating adipokines. Methods: Adiponectin, leptin and resistin were assayed in two groups of healthy controls, overweight and obese patients. The expression of ABCA1, ABCG1 and SR-BI in monocytes was measured. Cholesterol efflux from monocyte-derived macrophages was also determined. Results: Circulating adiponectin was decreased, whereas leptin and resistin were increased in overweight and obese patients compared with healthy controls. ABCA1 expression was significantly decreased in overweight and obese patients (Po0.01), whereas the levels of ABCG1 and SR-BI were comparable between the two groups. Adiponectin was correlated with ABCA1 (r ¼ 0.44, Po0.001), but not with ABCG1 and SR-BI. No associations between leptin, resistin and the expression of ABCA1, ABCG1 and SR-BI were found. Cholesterol efflux from monocyte-derived macrophages to apolipoprotein AI or to autologous serum was significantly impaired in overweight and obese patients, which were correlated with ABCA1 expression (r ¼ 0.47, Po0.001; r ¼ 0.43, Po0.001, respectively). Conclusion: The expression of ABCA1 in monocytes is reduced in overweight and obese patients, and the reduction in ABCA1 is associated with the impairment of cholesterol efflux from monocyte-derived macrophages.

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Section: Abca1 Expression In Obesitysupporting

confidence: 88%

Section: Abca1 Expression In Obesitysupporting

confidence: 88%

Section: Abca1 Expression In Obesitymentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The expression of ATP-binding cassette transporter A1 in Chinese overweight and obese patients

Zhou

Wang

et al. 2009

Int J Obes

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Biologic Activities

2011

High‐Density Lipoproteins

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Cannabinoids and Atherosclerotic Coronary Heart Disease

Singla

Sachdeva

Mehta

2012

Clinical Cardiology

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Marijuana is the most abused recreational drug in the United States. Cannabinoids, the active ingredients of marijuana, affect multiple organ systems in the human body. The pharmacologic effects of marijuana, based on stimulation of cannabinoid receptors CB1 and CB2, which are widely distributed in the cardiovascular system, have been well described. Activation of these receptors modulates the function of various cellular elements of the vessel wall, and may contribute to the pathogenesis of atherosclerosis. Clinically, there are reports linking marijuana smoking to the precipitation of angina and acute coronary syndromes. Recently, large published clinical trials with CB1 antagonist rimonabant did not show any significant benefit of this agent in preventing progression of atherosclerosis. In light of these findings and emerging data on multiple pathways linking cannabinoids to atherosclerosis, we discuss the literature on the role of cannabinoids in the pathophysiology of atherosclerosis. We also propose a marijuana paradox, which implies that inhalation of marijuana may be linked to precipitation of acute coronary syndromes, but modulation of the endocannabinoid system by a noninhalation route may have a salutary effect on the development of atherosclerosis.The authors have no funding, financial relationships, or conflicts of interest to disclose.

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Adiponectin prevents atherosclerosis by increasing cholesterol efflux from macrophages

Cited by 113 publications

References 14 publications

The expression of ATP-binding cassette transporter A1 in Chinese overweight and obese patients

The expression of ATP-binding cassette transporter A1 in Chinese overweight and obese patients

Biologic Activities

Cannabinoids and Atherosclerotic Coronary Heart Disease

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