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GLUT4 shows decreased levels in failing human adult hearts. We speculated that GLUT4 expression in cardiac muscle may be fine-tuned by microRNAs. Forced expression of miR-133 decreased GLUT4 expression and reduced insulin-mediated glucose uptake in cardiomyocytes. A computational miRNA target prediction algorithm showed that KLF15 is one of the targets of miR-133. It was confirmed that over-expression of miR-133 reduced the protein level of KLF15, which reduced the level of the downstream target GLUT4. Cardiac myocytes infected with lenti-decoy, in which the 3'UTR with tandem sequences complementary to miR-133 was linked to the luciferase reporter gene, had decreased miR-133 levels and increased levels of GLUT4. The expression levels of KLF15 and GLUT4 were decreased at the left ventricular hypertrophy and congestive heart failure stage in a rat model. The present results indicated that miR-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiomyocytes.
Pubmed ID: 19720047 RIS Download
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A database of experimentally verified microRNAs and miRNA target genes in human, mouse, rat, and other metazoan genomes. In addition to known miRNA targets, three computational tools previously developed, such as miRanda, RNAhybrid and TargetScan, were applied for identifying miRNA targets in 3'-UTR of genes. In order to reduce the false positive prediction of miRNA targets, several criteria are supported for filtering the putative miRNA targets. Furthermore, miRNA expression profiles can provide valuable clues for investigating the properties of miRNAs, such tissue specificity and differential expression in cancer/normal cell. Therefore, we performed the Q-PCR experiments for monitoring the expression profiles of 224 human miRNAs in eighteen major normal tissues in human. The cross-reference between the miRNA expression profiles and the expression profiles of its target genes can provide effective viewpoint to understand the regulatory functions of the miRNA.
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