Transcriptome Analysis of Mice Treated with Anti‐miR‐144

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Heart disease is a leading cause of death each year in the United States. In this study, we investigated the regulation of reverse cholesterol transport, a process shown to attenuate heart disease. Our lab has previously shown that mice treated with anti‐miR‐144 for 4 weeks increased ABCA1, which is involved in increased levels of high‐density lipoprotein and less fat in the heart. We hypothesized that long‐term treatment with anti‐miR‐144 would reveal other key genes in reverse cholesterol transport. Mice were placed on high fat, high cholesterol diet for 16 weeks, and treated with either saline, control anti‐miRNA, or anti‐miR‐144. Liver tissues were collected and processed for RNA sequencing. Using differential gene expression analysis, we found very few differences in gene expression among the treatment groups. When we did a comparison between the control‐treated mice and the anti‐miR‐144‐treated mice there was only one gene called MerTK that showed significant changes in gene expression. When we did a comparison between anti‐miR‐144‐treated mice and PBS‐treated mice, there were five genes that were shown to be differentially expressed which were Rgs3, Cd300lf, Fabp5, Dmac2l, and Slc1a3. Rgs3 and Slc1a3 showed higher expression in the PBS‐treated mice and the Cd300lf, Fabp5, Dmac2l showed higher expression in the anti‐miR‐144‐treated mice. As a reference, we did a comparison between the control‐treated mice and PBS‐treated mice and found that Cd300lf and the Fabp5 were also significantly expressed; this means that the changes for the two genes may not be due to anti‐miR‐144 treatment. Overall, we think that long‐term treatment of anti‐miR‐144 suppressed acute effects at the mRNA transcript level. Support or Funding Information UCLA, Bruins‐in‐Genomics Summer Program. Fisk University

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