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Mechanical stretch induced transcriptomic profiles in cardiac myocytes
Jaana Rysä1,2, Heikki Tokola3,4, Heikki Ruskoaho3,5
1School of Pharmacy, University of Eastern Finland, Kuopio, Finland. jaana.rysa@uef.fi.
Scientific Reports
|March 18, 2018
Summary
Mechanical forces trigger cardiac cell growth, but gene changes are unclear. This study reveals gene and microRNA alterations in stretched heart cells, identifying key regulators like Nrf2 and let-7 miRNAs involved in cardiac hypertrophy.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Genomics
Background:
- Mechanical forces induce cardiomyocyte hypertrophy in overloaded hearts.
- The precise transcriptional changes in cardiac myocytes due to mechanical stretch remain incompletely understood.
Purpose of the Study:
- To comprehensively analyze genome-wide gene expression and microRNA profiles in response to mechanical stretch in cultured neonatal rat ventricular myocytes.
- To identify regulatory networks and key molecules involved in mechanical stretch-induced cardiac hypertrophy.
Main Methods:
- Genome-wide time-series gene expression profiling of stretched neonatal rat ventricular myocytes (NRVMs).
- MicroRNA expression profiling of stretched NRVMs.
- Ingenuity Pathway Analysis for functional and upstream regulator prediction.
- Integration of mRNA and miRNA data to predict regulatory relationships.
Main Results:
- Identified significant differential expression of 205 to 1542 genes at various time points (1-48 hours) of cyclic mechanical stretch.
- Detected alterations in 8 microRNAs (1-12 hours) and 87 microRNAs (24-48 hours) in response to mechanical stretch.
- Predicted nuclear factor-like 2 (Nrf2), interferon regulatory transcription factors, and the let-7 miRNA family as key regulators of stretch-responsive genes.
Conclusions:
- Mechanical stretch induces significant time-dependent changes in both mRNA and miRNA expression in cardiomyocytes.
- Nrf2, interferon regulatory transcription factors, and let-7 miRNAs are predicted to play crucial roles in the molecular mechanisms underlying mechanical stretch-induced cardiac hypertrophy.
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