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The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

microRNA-483 ameliorates hypercholesterolemia by inhibiting PCSK9 production

Dong, Jianjie, He, Ming, Li, Jie, Pessentheiner, Ariane, Wang, Chen, Zhang, Jin, Sun, Yameng, Wang, Wei-Ting, Zhang, Yuqing, Liu, Junhui, Wang, Shen-Chih, Huang, Po-Hsun, Gordts, Philip L.S.M., Yuan, Zu-Yi, Tsimikas, Sotirios, Shyy, John Y.J.·2020·JCI Insight
DOI 10.1172/jci.insight.143812PMC PMC7714402
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Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) affects cholesterol homeostasis by targeting hepatic LDL receptor (LDLR) for lysosomal degradation. Clinically, PCSK9 inhibitors effectively reduce LDL-cholesterol (LDL-C) levels and the incidence of cardiovascular events. Because microRNAs (miRs) are integral regulators of cholesterol homeostasis, we investigated the involvement of miR-483 in regulating LDL-C metabolism. Using in silico analysis, we predicted that miR-483-5p targets the 3′-UTR of PCSK9 mRNA. In HepG2 cells, miR-483-5p targeted the PCSK9 3′-UTR, leading to decreased PCSK9 protein and mRNA expression, increased LDLR expression, and enhanced LDL-C uptake. In hyperlipidemic mice and humans, serum levels of total cholesterol and LDL-C were inversely correlated with miR-483-5p levels. In mice, hepatic miR-483 overexpression increased LDLR levels by targeting Pcsk9 , with a significant reduction in plasma total cholesterol and LDL-C levels. Mechanistically, the cholesterol-lowering effect of miR-483-5p was significant in mice receiving AAV8 PCSK9-3′-UTR but not Ldlr -knockout mice or mice receiving AAV8 PCSK9-3′-UTR (ΔBS) with the miR-483-5p targeting site deleted. Thus, exogenously administered miR-483 or similarly optimized compounds have potential to ameliorate hypercholesterolemia.

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Metadata

Authors
Dong, J., He, M., Li, J., Pessentheiner, A., Wang, C., Zhang, J., Sun, Y., Wang, W.-T., Zhang, Y., Liu, J., Wang, S.-C., Huang, P.-H., Gordts, P. L. S. M., Yuan, Z.-Y., Tsimikas, S., & Shyy, J. Y. J.
Affiliations
  • Department of Cardiology, First Affiliated Hospital, and
  • Division of Cardiology and
  • Cardiovascular Research Center, School of Basic Medical Sciences, First Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China.
  • Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, California, USA.
  • Department of Clinical Laboratory, First Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China.
  • Department of Anesthesiology,
  • Department of Critical Care Medicine, Taipei Veterans General Hospital, and
ORCID
Venue
JCI Insight
Publisher
American Society for Clinical Investigation
Published
2020-12-03
Volume
5
Issue
23
ISSN
2379-3708
DOI
10.1172/jci.insight.143812
PMC
PMC7714402
Cited by
53
References
8
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Institutes of Health (R01HL106579,R01HL108735)
  • National Natural Science Foundation of China (81941005)
  • National Key Research and Development Program grant (2018YFC1311500)
  • Key Project of Research and Development Plan of Shaanxi Province (2017ZDCXL-SF-02-04-01)
  • Ministry of Science and Technology, Taiwan (MOST 108-2633-B-009-001)
  • Academic Senate, University of California, San Diego (RG096470)
  • Foundation Leducq (16CVD01)

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