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Versican accumulation drives Nos2 induction and aortic disease in Marfan syndrome via Akt activation.

EMBO molecular medicine·2024
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Increased Proteoglycanases in Pulmonary Valves after Birth Correlate with Extracellular Matrix Maturation and Valve Sculpting.

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Updated: Jan 16, 2026

En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
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ADAMTS5 Orchestrates Cell Lineage Specific Patterning and Extracellular Matrix Organization During Semilunar Valve

Loren E Dupuis1, Joshua J Mifflin1, Amy L Marston1

  • 1Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.

Journal of Cardiovascular Development and Disease
|September 26, 2025
PubMed
Summary

Proteoglycan cleavage by Adamts5 is crucial for normal aortic valve development. Its absence causes Versican accumulation and abnormal valve morphology, suggesting new therapeutic targets for aortic valve disease.

Keywords:
ADAMTS5EndoMTaortic valvecardiac neural crestextracellular matrixproteoglycansemilunar valvesvalvular interstitial cellsversican

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Area of Science:

  • Cardiovascular Biology
  • Extracellular Matrix Biology
  • Developmental Biology

Background:

  • Aortic valve disease affects 5% of the aging population, with replacement as the sole treatment.
  • Dysfunctional aortic valves show increased extracellular matrix (ECM) proteoglycans.
  • Versican (VCAN) proteoglycan levels are regulated by ECM proteolytic cleavage.

Purpose of the Study:

  • To investigate if Versican (VCAN) cleavage by Adamts5 is essential for cell behaviors and ECM organization during aortic valve development.
  • To determine the role of Adamts5 in cardiac neural crest (CNC) and endothelial-mesenchymal transition (EndoMT) lineages during aortic valve formation.

Main Methods:

  • Cardiac neural crest (CNC) lineage tracing in mice lacking Adamts5.
  • Utilized Adamts5 floxed mice to assess gene function in specific cell types.
  • Analyzed Versican accumulation, ECM stratification, and semilunar valve (SLV) morphology.

Main Results:

  • Mice lacking Adamts5 displayed disorganized CNC patterning, excess VCAN, and enlarged semilunar valves.
  • Adamts5 is required in endothelial cells and their mesenchymal derivatives (EndoMT lineage) to control VCAN levels and ECM stratification.
  • Loss of Adamts5 function leads to abnormal aortic valve morphology.

Conclusions:

  • VCAN cleavage by Adamts5 is a key ECM remodeling event orchestrating cell behaviors and proteoglycan levels during aortic valve development.
  • Understanding VCAN regulation may reveal therapeutic targets for aortic valve disease.
  • Adamts5 plays a critical role in maintaining aortic valve structure and function.