Abstract:MicroRNAs (miRNAs) regulate many aspects of human biology. They target mRNAs for translational repression or degradation through base-pairing with 3’ UTRs, primarily via seed sequences (nucleotides 2-8 in the mature miRNA sequence). A number of individual miRNAs and miRNA families share seed sequences and targets, but differ in the sequences outside of the seed. miRNAs have been implicated in the etiology of a wide variety of human diseases and therefore represent promising therapeutic targets. However, potent… Show more
“…Three distinct miR-26 loci (Mir26a1, Mir26a2, and Mir26ab) within the mouse genome render genetic loss of function difficult (27). Previous studies in mice and nonhuman primates have supported the feasibility of LNA antisense approaches to modulating miR pathways that have important physiological consequences in vivo (30,31). We therefore intraperitoneally injected CD-fed WT mice with PBS (vehicle) or LNA-miR-26a antisense (miR-26a inhibitor).…”
“…Three distinct miR-26 loci (Mir26a1, Mir26a2, and Mir26ab) within the mouse genome render genetic loss of function difficult (27). Previous studies in mice and nonhuman primates have supported the feasibility of LNA antisense approaches to modulating miR pathways that have important physiological consequences in vivo (30,31). We therefore intraperitoneally injected CD-fed WT mice with PBS (vehicle) or LNA-miR-26a antisense (miR-26a inhibitor).…”
“…miR-33 was one of the earliest identified miRNAs to regulate cholesterol homeostasis, and much of the research involving this miRNA has focused on its role in repressing cholesterol efflux and plasma levels of HDL-C by targeting ABCA1 (52). Studies in mice and nonhuman primates showed that miR-33 inhibitors increase plasma levels of HDL (24)(25)(26)(30)(31)(32), a lipoprotein whose plasma level in observational studies is inversely associated with cardiovascular risk, suggesting that it may hold value as a therapeutic target for atherosclerosis. Indeed, a previous study of Ldlr -/-mice with established atherosclerotic plaques that were treated with anti-miR-33 in conjunction with chow diet showed increased plasma levels of HDL-C and regression of atherosclerosis (31).…”
Section: Group) (G and H) Flow Cytometric Analysis Of Aldh Activity mentioning
“…Recent studies provide considerable evidence about the effect of miR-33 s on lipid metabolism, particularly in the preclinical stage. 49 Because one miRNA can have many targets and affect the expression levels of many genes, further investigations are required to understand the complexity of miRNA biology. In the case of the miR-33s, complete inhibition leads to the development of obesity and liver steatosis; 29 therefore, spatiotemporal regulation may be required.…”
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