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Erratum Free access | 10.1172/JCI70146

Myeloid cell–specific serine palmitoyltransferase subunit 2 haploinsufficiency reduces murine atherosclerosis

Mahua Chakraborty, Caixia Lou, Chongmin Huan, Ming-Shang Kuo, Tae-Sik Park, Guoqing Cao, and Xian-Cheng Jiang

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Published May 1, 2013 - More info

Published in Volume 123, Issue 5 on May 1, 2013
J Clin Invest. 2013;123(5):2332–2332. https://doi.org/10.1172/JCI70146.
© 2013 The American Society for Clinical Investigation
Published May 1, 2013 - Version history
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Myeloid cell–specific serine palmitoyltransferase subunit 2 haploinsufficiency reduces murine atherosclerosis
Mahua Chakraborty, … , Guoqing Cao, Xian-Cheng Jiang
Mahua Chakraborty, … , Guoqing Cao, Xian-Cheng Jiang
Research Article Cardiology

Myeloid cell–specific serine palmitoyltransferase subunit 2 haploinsufficiency reduces murine atherosclerosis

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Abstract

Serine palmitoyltransferase (SPT) is the first and rate-limiting enzyme of the de novo biosynthetic pathway of sphingomyelin (SM). Both SPT and SM have been implicated in the pathogenesis of atherosclerosis, the development of which is driven by macrophages; however, the role of SPT in macrophage-mediated atherogenesis is unknown. To address this issue, we have analyzed macrophage inflammatory responses and reverse cholesterol transport, 2 key mediators of atherogenesis, in SPT subunit 2–haploinsufficient (Sptlc2+/–) macrophages. We found that Sptlc2+/– macrophages have significantly lower SM levels in plasma membrane and lipid rafts. This reduction not only impaired inflammatory responses triggered by TLR4 and its downstream NF-κB and MAPK pathways, but also enhanced reverse cholesterol transport mediated by ABC transporters. LDL receptor–deficient (Ldlr–/–) mice transplanted with Sptlc2+/– bone marrow cells exhibited significantly fewer atherosclerotic lesions after high-fat and high-cholesterol diet feeding. Additionally, Ldlr–/– mice with myeloid cell–specific Sptlc2 haploinsufficiency exhibited significantly less atherosclerosis than controls. These findings suggest that SPT could be a novel therapeutic target in atherosclerosis.

Authors

Mahua Chakraborty, Caixia Lou, Chongmin Huan, Ming-Shang Kuo, Tae-Sik Park, Guoqing Cao, Xian-Cheng Jiang

×

Original citation: J. Clin. Invest. 2013;123(4):1784–1797. doi:10.1172/JCI60415.

Citation for this erratum: J. Clin. Invest. 2013;123(5):2332. doi:10.1172/JCI70146.

During the processing of this manuscript, the Western blot in Figure 3D was labeled incorrectly. The correct figure is below.

Figure 3

The JCI regrets the error.

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  • Version 1 (May 1, 2013): No description

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