Author
Listed:
- Katey J. Rayner
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Christine C. Esau
(Regulus Therapeutics)
- Farah N. Hussain
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Allison L. McDaniel
(Wake Forest University School of Medicine)
- Stephanie M. Marshall
(Wake Forest University School of Medicine)
- Janine M. van Gils
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Tathagat D. Ray
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Frederick J. Sheedy
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Leigh Goedeke
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Xueqing Liu
(Regulus Therapeutics)
- Oleg G. Khatsenko
(Regulus Therapeutics)
- Vivek Kaimal
(Regulus Therapeutics)
- Cynthia J. Lees
(Wake Forest University School of Medicine)
- Carlos Fernandez-Hernando
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Edward A. Fisher
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
- Ryan E. Temel
(Wake Forest University School of Medicine)
- Kathryn J. Moore
(Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine)
Abstract
Manipulating plasma lipids Recent work in mice has shown that microRNA-33a is an important regulator of lipid metabolism and that its inhibition can increase plasma high-density lipoprotein (HDL) and decrease atherosclerosis. Rayner et al. take an important step in translating these findings to non-human primates (African green monkeys), which, like humans and unlike mice, express both miR-33a and miR-33b. They find that anti-miR-33 is effective at inhibiting both miR-33a and miR-33b. As seen in the mouse studies, anti-miR33 raised plasma HDL but had the additional beneficial effect of reducing very low-density lipoprotein triglycerides, making this type of 'antagomir' therapy a candidate method of treating dyslipidaemias that increase cardiovascular disease risk.
Suggested Citation
Katey J. Rayner & Christine C. Esau & Farah N. Hussain & Allison L. McDaniel & Stephanie M. Marshall & Janine M. van Gils & Tathagat D. Ray & Frederick J. Sheedy & Leigh Goedeke & Xueqing Liu & Oleg G, 2011.
"Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides,"
Nature, Nature, vol. 478(7369), pages 404-407, October.
Handle:
RePEc:nat:nature:v:478:y:2011:i:7369:d:10.1038_nature10486
DOI: 10.1038/nature10486
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Citations
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Cited by:
- Nathan L. Price & Pablo Fernández-Tussy & Luis Varela & Magdalena P. Cardelo & Marya Shanabrough & Binod Aryal & Rafael Cabo & Yajaira Suárez & Tamas L. Horvath & Carlos Fernández-Hernando, 2024.
"microRNA-33 controls hunger signaling in hypothalamic AgRP neurons,"
Nature Communications, Nature, vol. 15(1), pages 1-13, December.
- Nicolas Greliche & Tanja Zeller & Philipp S Wild & Maxime Rotival & Arne Schillert & Andreas Ziegler & Panos Deloukas & Jeanette Erdmann & Christian Hengstenberg & Willem H Ouwehand & Nilesh J Samani , 2012.
"Comprehensive Exploration of the Effects of miRNA SNPs on Monocyte Gene Expression,"
PLOS ONE, Public Library of Science, vol. 7(9), pages 1-12, September.
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