Interdependent changes of nuclear lamins, nuclear pore complexes, and ploidy regulate cellular regeneration and

Yao Li1,2, Alberto Bertozzi1,2, Mellissa Rw Mann3,4

  • 1Division of Pediatric Cardiology, Pediatric Institute for Heart Regeneration and Therapeutics (I-HRT), UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.

Nucleus (Austin, Tex.)
|August 22, 2023
PubMed

Insights

Adult mammalian heart muscle cells (cardiomyocytes) lose regenerative capacity due to polyploidy. This study reveals how nuclear lamina and pore complex changes during maturation impact cardiomyocyte regeneration and stress response.

Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Molecular Biology

Background:

  • Adult mammalian cardiomyocytes are typically post-mitotic and polyploid, limiting heart regeneration.
  • Fetal and neonatal cardiomyocytes are diploid and proliferative, contributing to heart development and repair.

Purpose of the Study:

  • To investigate the interdependent changes in nuclear lamina, nuclear pore complexes, and ploidy during cardiomyocyte maturation.
  • To understand how these nuclear alterations affect gene regulation, nuclear transport, and cellular regeneration in the heart.

Main Methods:

  • Analysis of nuclear lamina and nuclear pore complex alterations in cardiomyocytes.
  • Assessment of DNA content (ploidy) changes during heart muscle cell maturation.
  • Investigation of the functional consequences for nuclear transport and gene regulation.

Main Results:

  • Identified interdependent changes in the nuclear lamina, nuclear pore complexes, and DNA content during cardiomyocyte maturation.
  • Demonstrated how nuclear lamina modifications influence nuclear pore complexes in heart muscle cells.
  • Linked these nuclear changes to altered nuclear transport and gene regulation.

Conclusions:

  • Cardiomyocyte maturation involves coordinated changes in nuclear structure and ploidy.
  • These nuclear alterations are critical for regulating gene expression and cellular function, impacting heart regeneration and stress response.

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