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Regulus Therapeutics and Collaborators Publish New Pre-Clinical Data on microRNA-33 Demonstrating Key Role in Cholesterol Homeostasis and Fatty Acid Metabolism
Date:10/20/2011

ts the benefits of modulating miR-33a/b and their downstream metabolic pathways."

The Nature paper, "Inhibition of miR-33a/b in non-human primates raises plasma HDL cholesterol and reduces VLDL triglycerides," showed that systemic delivery of an anti-miR targeting both miR-33a and miR-33b in non-human primates increased hepatic miR-33 target gene expression and induced a sustained increase in plasma HDL-C over the 12-week study. In the study protocol, six animals per group received anti-miR-33 via subcutaneous injection at a clinically relevant dose of five mg/kg or a mismatch control. The anti-miR or control were formulated in saline, and administered twice weekly for the first two weeks, and then weekly for the remainder of the 12-week study.  Results showed a maximal HDL-C increase of 50% after eight weeks that was sustained throughout the remainder of the study. Anti-miR-33a/b treatment in this model also increased the expression of miR-33 target genes involved in fatty acid oxidation resulting in suppressed triglyceride levels, a finding not previously observed in mice. The decrease in triglycerides was apparent after four weeks and reached a maximum reduction of 50%.  This pre-clinical study was the first to demonstrate that inhibiting miR-33a/b has a profound and sustained effect on both circulating HDL-C and plasma triglyceride levels.

Ryan Temel, Ph.D., assistant professor at Wake Forest Baptist Medical Center, said, "anti-miR-33a/b has the potential to treat multiple aspects of metabolic syndrome which is a group of risk factors that increase the risk for coronary artery disease, stroke, and type 2 diabetes."

Multiple studies have demonstrated that miR-33a/b strongly represses the cholesterol transporter ABCA1, resulting in decreased generation of HDL-C and reverse cholesterol transport (Rayner et al., J Clin Invest. 2011) as well as key enzymes involved in the oxidation of fatty acid resulting in the acc
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