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sox9b is required in cardiomyocytes for cardiac morphogenesis and function.

Joseph C Gawdzik1,2, Monica S Yue1,2, Nathan R Martin3

  • 1Molecular and Environmental Toxicology Center, University of Wisconsin at Madison, Madison, WI, USA.

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SOX9b is crucial for heart development. Inhibiting SOX9b in cardiomyocytes disrupts heart structure and function, leading to heart failure and impacting key cardiac genes.

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Area of Science:

  • Developmental biology
  • Cardiovascular research
  • Toxicology

Background:

  • High mobility group transcription factor SOX9 is vital in stem cells and organ development.
  • Environmental toxicants can downregulate SOX9 and zebrafish sox9b, disrupting organogenesis.
  • SOX9/sox9b dysfunction leads to developmental defects and health issues.

Purpose of the Study:

  • To investigate the role of sox9b in cardiomyocyte development and function.
  • To examine the effects of inhibiting sox9b specifically in cardiomyocytes using a dominant-negative approach.

Main Methods:

  • Generated a dominant-negative sox9b (dnsox9b) construct.
  • Utilized the Gal4/UAS system for cardiomyocyte-specific expression of dnsox9b in zebrafish.
  • Assessed cardiac morphology, function (echocardiography), and gene expression (RT-qPCR).

Main Results:

  • Cardiomyocyte-specific sox9b inhibition caused reduced ventricular cardiomyocytes and increased atrial cardiomyocytes.
  • Impaired epicardial development and hypoplastic endothelial cushions were observed.
  • Cardiac function was compromised, with decreased stroke volume, ejection fraction, and cardiac output.
  • Expression of key cardiac development genes (nkx2.5, nkx2.7, myl7) and c-fos was significantly reduced.

Conclusions:

  • SOX9b transcriptional regulation is essential for normal cardiomyocyte development.
  • Disruption of sox9b function in cardiomyocytes leads to cardiac abnormalities and heart failure.
  • Environmental disruption of SOX9b may contribute to cardiac developmental disorders.