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Updated: Jul 17, 2026
08:03
In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
Versican proteolysis mediates myocardial regression during outflow tract development
Christine B Kern1, Russell A Norris, Robert P Thompson
1Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, SC 29425-2204, USA. kernc@musc.edu
Summary
Versican proteolysis is crucial for cardiac outflow tract remodeling. Its cleavage fragments promote smooth muscle replacement by reducing myocardial cell association and thickness during development.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Extracellular Matrix Biology
Background:
- Cardiac outflow tract (OFT) remodeling involves replacing the myocardial sleeve with smooth muscle.
- Versican, a proteoglycan, is downregulated during distal OFT remodeling.
- Increased production of versican's N-terminal fragment (G1) coincides with myocardial loss.
Purpose of the Study:
- To investigate the role of versican proteolysis in OFT remodeling.
- To determine the effects of specific versican isoforms on OFT myocardial development.
Main Methods:
- Adenoviral-mediated expression of a non-cleavable versican isoform (V3) and the G1 fragment in vivo.
- In vitro studies using cultured primary cardiomyocytes.
- Assessment of myocardial layer thickness, cell association, and proliferation.
Main Results:
- V3 expression increased proximal OFT myocardial layer thickness without affecting proliferation.
- G1 domain expression led to thinning and interruptions in the OFT myocardium.
- In vitro, V3 promoted cardiomyocyte cell-cell association, while G1 disrupted it.
Conclusions:
- Intact versican and its G1 cleavage product exert opposing effects on myocardial cells.
- Versican proteolysis likely facilitates the loss of distal myocardium during OFT remodeling.
- Targeting versican processing may offer therapeutic avenues for cardiac development disorders.
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