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The novel role and underlying mechanism of Wnt5a in regulating cellular cholesterol accumulation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Qin, Li Hu, Rong Zhu, Neng Yao, Hai-Lun Lei, Xiao-Yong Li, Shun-Xiang Liao, Duan-Fang Zheng, Xi-Long
Description	Country affiliation: China Author Affiliation: Qin L ( Division of Stem Cell Regulation and Application, School of Pharmacy, Hunan University of Chinese Medicine, Changsha, China)
Abstract	Cholesterol accumulation is a critical step during the development and progression of atherosclerosis. Recently, Wnt5a expression has been found to be markedly upregulated in both murine and human atherosclerotic lesions. However, the effect and mechanism of Wnt5a in atherosclerosis is poorly understood. In the present study, we investigated the effects and potential mechanisms of Wnt5a on cholesterol accumulation during atherosclerosis. We used RAW264.7 and vascular smooth muscle cells (VSMC) treated with oxidized low-density lipoprotein (oxLDL) as lipid-loaded cell models. We found that expression of Wnt5a protein was increased in a concentration (25, 50, 75 and 100 µg/mL)- and time (24, 48 and 72 h)-dependent manner by oxLDL treatment. To explore the underlying mechanism, we used Wnt5a short interference (si) RNA to knockdown Wnt5a expression in both RAW264.7 cells and VSMC, or applied recombinant Wnt5a (rWnt5a) to stimulate Wnt5a signalling. After Wnt5a knockdown, total cholesterol (TC) and free cholesterol (FC) content in both cell types increased significantly (P < 0.05) upon exposure to oxLDL. Conversely, the TC and FC content decreased markedly (P < 0.05) after treatment of cells with rWnt5a. More importantly, both protein and mRNA expression of Caveolin-1 and ATP-binding cassette transporter A1 (ABCA1) was significantly reduced after exposure of wnt5a siRNA-treated cells to oxLDL, whereas rWnt5a treatment of cells resulted in increased Caveolin-1 and ABCA1 protein expression after exposure of cells to oxLDL. Together, these findings demonstrate, for the first time, that Wnt5a reduces the accumulation of cholesterol in lipid-loaded cells by regulating the mRNA expression of Caveolin-1 and ABCA1, which are involved in reverse cholesterol transport. This may present a novel mechanism of Wnt5a-mediated cholesterol transportation in macrophages and VSMC. Therefore, targeting the Wnt5a signalling pathway may have clinical implications in atherosclerosis.
File Format	HTM / HTML
ISSN	03051870
Issue Number	9
Volume Number	41
e-ISSN	14401681
Journal	Clinical and Experimental Pharmacology and Physiology
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2014-09-01
Publisher Place	Australia
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Physiology Discipline Pharmacology Cholesterol Metabolism Wnt Proteins Atp Binding Cassette Transporter 1 Biosynthesis Animals Atherosclerosis Caveolin 1 Cells, Cultured Dose-response Relationship, Drug Gene Expression Regulation Drug Effects Gene Knockdown Techniques Lipoproteins, Ldl Pharmacology Male Mice Rna, Small Interfering Rats Genetics Wnt Signaling Pathway Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Pharmacology

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The novel role and underlying mechanism of Wnt5a in regulating cellular cholesterol accumulation.