Abstract 19631: MicroRNAs Modulation in a Mice Model of Physiological Left Ventricular Hypertrophy
INTRODUCTION: Physiological left ventricular hypertrophy (LVH) has distinct phenotypic adaptations that might me modulated by microRNAs (miRs) which are fine-tune regulators of gene expression. We tested the hypothesis that physiological LVH has differential miRs expression in mice subjected to a voluntary exercise protocol.
METHODS: Balb/c mice were kept in cages with exercising wheels (Exercise group - EXE; n=15 sacrificed on day 7 and n=17 sacrificed 35 days after training) or in cages without wheels (Sedentary group - SED; n=12 in each time point). LVH was evaluated by the left ventricular weight/body weight ratio (LVW/BW). MiRs were extracted with miRNeasy kit (Qiagen, USA). A microRNA microarray based on the miRBase version 16 (LC Sciences, Houston, Texas, EUA) was carried out using a pool of miRs extracted from the LV. After miR extraction, 50 pM of synthetic cel-miR-39 were spiked-in as a standard control. RT-qPCR was performed with microRNA Reverse Transcription Kit® and TaqMan Probes® (Applied Biosystems Inc., USA).
RESULTS: After 7 days of training there was an increase of 7% in LVW/BW ratio on EXE compared to SED group (3.6±0.2 vs. 3.3±0.1, respectively; p=0.004) and this result was sustained at 35 days (12% increase; 3.7±0.2 vs. 3.3±0.1, respectively; p<0.001). 7 DAYS analyses: expression of miR-26b and miR-143 was decreased in the EXE compared to the SED group (0.5-fold, p=0.017 and 0.7-fold, p=0.018, respectively). miR-150 showed an increased expression in the EXE group (3.0-fold, p=0.001). 35 DAYS analyses: expression of miR-27a was down-regulated (0.8-fold, p=0.03), while miR-150 was up-regulated (1.9-fold, p=0.016) in the EXE group. miRs previously described to be involved in cardiovascular diseases (miR-21, miR-195 and miR-499) were similar between groups.
CONCLUSIONS: Our data suggest that physiological LVH was associated to significant modulation of miRs that might regulate affect metabolic adaptations (miR-26b:GSK3B) and apoptosis pathway activation (miR-150:FOXO4). Also miRs could have an effect on cellular growth and hypertrophy (miR-27a:IGF1 and miR-143:MTPN).
- © 2012 by American Heart Association, Inc.