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A SOX17-PDGFB signaling axis regulates aortic root development.

Pengfei Lu1, Ping Wang1,2, Bingruo Wu1

  • 1Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA.

Nature Communications
|July 13, 2022
PubMed
Summary

Sox17 gene deletion in mice causes underdeveloped aortic roots, leading to bicuspid aortic valves and abnormal coronary arteries. Restoring PDGFB signaling rescues these congenital heart defects.

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Protein Isolation from the Developing Embryonic Mouse Heart Valve Region
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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Genetics

Background:

  • Congenital aortic root abnormalities, including bicuspid aortic valves and anomalous coronary arteries, have unknown developmental origins.
  • Understanding the genetic and molecular mechanisms is crucial for addressing these complex heart defects.

Purpose of the Study:

  • To investigate the role of Sox17 in the development of the aortic root and associated structures.
  • To elucidate the molecular pathways involved in Sox17-mediated aortic root patterning.

Main Methods:

  • Utilized a mouse model with targeted deletion of the Sox17 gene in aortic root endothelium.
  • Analyzed aortic root morphology, valve formation, and coronary ostium positioning.
  • Investigated gene expression, specifically focusing on Pdgfb and PDGFB signaling pathways.
  • Performed rescue experiments by restoring PDGFB expression.

Main Results:

  • Sox17 deletion resulted in an underdeveloped aortic root, absence of the non-coronary leaflet, and a mispositioned left coronary ostium.
  • These defects were linked to reduced proliferation of mesenchyme and smooth muscle cells derived from the second heart field.
  • Sox17 was found to regulate Pdgfb transcription via an enhancer element, inhibiting endothelial Pdgfb expression and downstream PDGFB signaling.
  • Restoration of PDGFB in the aortic root endothelium rescued the observed developmental defects.

Conclusions:

  • A SOX17-PDGFB signaling axis is critical for normal aortic root development, including aortic valve and coronary ostium patterning.
  • This pathway may represent a shared mechanism underlying concurrent anomalous aortic valve and coronary artery diseases.
  • Findings provide insights into the etiology of complex congenital heart abnormalities.