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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
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Sox17 is required for normal pulmonary vascular morphogenesis.

Alexander W Lange1, Hans Michael Haitchi2, Timothy D LeCras1

  • 1Perinatal Institute, Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, The University of Cincinnati College of Medicine, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, United States.

Developmental Biology
|January 15, 2014
PubMed
Summary
This summary is machine-generated.

Sox17 is crucial for lung vascular development. Its absence causes severe pulmonary vascular defects and postnatal cardiovascular problems, highlighting its role in cardiovascular homeostasis.

Keywords:
Dermo1-CreEndothelialLungSox17Vascular morphogenesis

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Area of Science:

  • Developmental Biology
  • Cardiovascular Biology
  • Pulmonary Biology

Background:

  • Sox17 is a transcription factor vital for embryonic development, including endoderm formation and vascular morphogenesis.
  • In the lung, Sox17 expression is observed in embryonic pulmonary vasculature progenitors and mature vascular endothelial cells.

Purpose of the Study:

  • To investigate the role of Sox17 in pulmonary vascular development and postnatal cardiovascular homeostasis.
  • To determine the consequences of Sox17 deletion in the developing pulmonary vasculature.

Main Methods:

  • Conditional deletion of Sox17 in splanchnic mesenchyme-derivatives using Dermo1-Cre.
  • Analysis of pulmonary vascular abnormalities in Sox17-deficient mice before and after birth.
  • Assessment of postnatal cardiovascular phenotypes, including cardiac function and survival.

Main Results:

  • Conditional deletion of Sox17 led to significant loss of the protein in pulmonary vascular endothelial cells.
  • Mice lacking Sox17 exhibited prenatal pulmonary vascular abnormalities such as varices, enlarged arteries, and reduced microvascular perfusion.
  • Postnatal lethality was observed in Sox17-deficient mice, accompanied by decreased microvascular density, alveolar simplification, cardiac hypertrophy, and valvular regurgitation.

Conclusions:

  • Sox17 is essential for the normal formation of the pulmonary vasculature.
  • Sox17 plays a critical role in maintaining postnatal cardiovascular homeostasis.
  • Pulmonary vascular defects resulting from Sox17 deficiency significantly impact postnatal cardiac function and survival.