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Tead1 is required for perinatal cardiomyocyte proliferation

Ruya Liu1,2, Rajaganapathi Jagannathan3, Feng Li1

  • 1Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.

Plos One
|February 28, 2019
PubMed

Insights

The transcription factor Tead1 is essential for cardiomyocyte proliferation during the perinatal period. Its deletion leads to lethal dilated cardiomyopathy in mice due to reduced cell division.

Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Molecular Cardiology

Background:

  • Adult heart size depends on cardiomyocyte number and size, established during early development.
  • The Hippo kinase pathway regulates cardiomyocyte proliferation, with Tead1 as a key downstream factor.
  • The specific role of Tead1 in perinatal cardiomyocyte proliferation remains unclear.

Purpose of the Study:

  • To investigate the role of the transcription factor Tead1 in perinatal cardiomyocyte proliferation.
  • To determine the consequences of Tead1 deletion in cardiomyocytes during the perinatal period.

Main Methods:

  • Generation of cardiomyocyte-specific perinatal Tead1 knockout mice (Tead1-cKO) using Myh6-Cre.
  • Analysis of Tead1-cKO mice for lethality, cardiac function, and cardiomyocyte proliferation.
  • In vitro studies using HL-1 cardiac cell line to confirm cell-autonomous Tead1 function.

Main Results:

  • Perinatal deletion of Tead1 resulted in lethal dilated cardiomyopathy by postnatal day 9.
  • Tead1-deficient cardiomyocytes exhibited significantly decreased proliferation during the critical postnatal period.
  • Tead1 deficiency led to reduced levels of cell cycle-promoting proteins in cardiomyocytes.
  • Cell-autonomous function of Tead1 is required for normal cardiomyocyte proliferation.

Conclusions:

  • Tead1 plays a critical, non-redundant role in regulating cardiomyocyte proliferation during the perinatal period.
  • Tead1 is essential for maintaining cardiomyocyte cell cycle progression by controlling key regulatory proteins.
  • Disruption of Tead1 function leads to impaired heart development and dilated cardiomyopathy.

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