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Updated: May 1, 2026
Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization
Published on: September 15, 2018
An analysis of the global expression of microRNAs in an experimental model of physiological left ventricular
Nidiane C Martinelli1, Carolina R Cohen1, Kátia G Santos2
1Experimental and Molecular Cardiovascular Laboratory and the Heart Failure and Cardiac Transplant Unit from the Cardiology Division at Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil; Post-Graduate Program in Cardiology and Cardiovascular Science, Porto Alegre, RS, Brazil; Post-Graduate Program in Genetics and Molecular Biology at the Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil.
Background:
MicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Studies of transgenic mouse models have indicated that deregulation of a single miR can induce pathological cardiac hypertrophy and cardiac failure. The roles of miRs in the genesis of physiological left ventricular hypertrophy (LVH), however, are not well understood.
Objective:
To evaluate the global miR expression in an experimental model of exercise-induced LVH.
Methods:
Male Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed on an odometer-monitored metal wheels for 35 days. Various tests were performed after 7 and 35 days of training, including a transthoracic echocardiography, a maximal exercise test, a miR microarray (miRBase v.16) and qRT-PCR analysis.
Results:
The ratio between the left ventricular weight and body weight was increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at day 35 of training (p<0.001). After 7 days of training, the microarray identified 35 miRs that were differentially expressed between the two groups: 20 were up-regulated and 15 were down-regulated in the EXE group compared with the SED group (p = 0.01). At day 35 of training, 25 miRs were differentially expressed: 15 were up-regulated and 10 were decreased in the EXE animals compared with the SED animals (p<0.01). The qRT-PCR analysis demonstrated an increase in miR-150 levels after 35 days and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise.
Conclusions:
We have identified new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, -27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not changed in physiological LVH.
Insights
Exercise-induced cardiac hypertrophy involves specific microRNAs (miRs). This study identified novel miRs, including miR-26b, miR-150, miR-27a, and miR-143, that modulate physiological left ventricular hypertrophy (LVH) in mice.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRs) are small non-coding RNAs regulating gene expression.
- Deregulation of single miRs can cause pathological cardiac hypertrophy and failure.
- The role of miRs in physiological left ventricular hypertrophy (LVH) remains unclear.
Purpose of the Study:
- To investigate global microRNA expression in an experimental model of exercise-induced LVH.
- To identify specific miRs involved in physiological cardiac adaptation to exercise.
Main Methods:
- Male Balb/c mice were subjected to 35 days of voluntary wheel exercise.
- Transthoracic echocardiography and maximal exercise tests were performed.
- MicroRNA expression was analyzed using microarray and qRT-PCR at 7 and 35 days.
Main Results:
- Exercise significantly increased left ventricular weight relative to body weight.
- Microarray analysis revealed differential expression of 35 miRs at day 7 and 25 miRs at day 35.
- qRT-PCR confirmed changes in miR-150, miR-26b, miR-27a, and miR-143 levels.
Conclusions:
- New miRs, including miR-26b, -150, -27a, and -143, modulate physiological cardiac hypertrophy.
- Regulatory pathways for pathological LVH appear unaltered in physiological LVH induced by exercise.
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