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11:46
Axon Stretch Growth: The Mechanotransduction of Neuronal Growth
Published on: August 10, 2011
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miR-486 is modulated by stretch and increases ventricular growth.
Stephan Lange1,2, Indroneal Banerjee1, Katrina Carrion3
1Division of Cardiovascular Medicine, Department of Medicine, UCSD School of Medicine, San Diego, California, USA.
JCI Insight
|September 13, 2019
Summary
Mechanical stress during heart development can cause congenital heart defects. This study found that microRNA-486 (miR-486) responds to stretch and promotes ventricle growth, offering potential therapeutic targets for conditions like hypoplastic left heart syndrome.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Molecular Cardiology
Background:
- Biomechanical stimuli are crucial for normal cardiac development.
- Disruptions in these stimuli can lead to congenital cardiac defects, including hypoplastic left heart syndrome (HLHS).
- Understanding the molecular pathways responding to mechanical stress is vital for addressing these conditions.
Purpose of the Study:
- To identify stretch-responsive molecular pathways involved in cardiac development.
- To investigate the role of microRNA-486 (miR-486) in response to mechanical stretch.
- To explore the potential of miR-486 as a therapeutic target for cardiac growth.
Main Methods:
- Utilized miRNA sequencing (miRNA-Seq) to identify stretch-responsive miRNAs in cardiomyocytes.
- Analyzed miR-486 levels in right ventricles (RVs) from HLHS patients and dilated sheep RVs.
- Administered miR-486 mimic to newborn mice to assess effects on left ventricle size and cardiomyocyte proliferation.
- Examined downstream signaling pathways including FoxO1, Smad, Stat1, Gata-4, and Srf.
Main Results:
- miR-486 expression increased in cardiomyocytes subjected to cyclic stretch.
- A trend toward higher miR-486 levels was observed in RVs from HLHS patients.
- Dilated sheep RVs showed significantly increased miR-486 levels.
- In vivo administration of miR-486 mimic resulted in larger left ventricles and increased cardiomyocyte proliferation in mice.
- miR-486 modulated signaling pathways, decreasing FoxO1 and Smad, and increasing Stat1, Gata-4, and Srf.
Conclusions:
- miR-486 is a novel stretch-responsive microRNA involved in cardiac development.
- Increased miR-486 promotes ventricle growth and cardiomyocyte proliferation.
- This study presents the first evidence of a stretch-responsive miRNA that enhances ventricular growth in vivo.
- miR-486 represents a potential therapeutic target for congenital heart defects characterized by altered biomechanical forces.
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