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Related Experiment Video

Updated: Jun 18, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

E2F4 is required for cardiomyocyte proliferation.

Machteld J van Amerongen¹, Florian Diehl, Tatyana Novoyatleva

¹Department of Cardiac Development and Remodelling, Excellence Cluster Cardio-Pulmonary System, Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, Bad Nauheim 61231, Germany.

Cardiovascular Research

|December 4, 2009

Summary

This summary is machine-generated.

The transcription factor E2F4 is crucial for cardiomyocyte proliferation and mitosis during heart development. Inhibition of E2F4 significantly reduces mitosis in postnatal cardiomyocytes.

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Published on: November 13, 2015

Area of Science:

Cardiovascular Biology
Molecular Cell Biology
Developmental Biology

Background:

The E2F transcription factor family regulates cell proliferation.
The specific role of E2F4 in cell proliferation is debated, with evidence suggesting both inhibitory and activating functions.
Its function during heart development and in cardiomyocytes remains largely uncharacterized.

Purpose of the Study:

To investigate the role of E2F4 in heart development.
To elucidate the function of E2F4 in proliferating cardiomyocytes.

Main Methods:

Quantitative analysis of nuclear E2F4 expression during mouse heart development and in postnatal cardiomyocytes.
siRNA-mediated knockdown of E2F4 in proliferating cardiomyocytes.
Assessment of DNA synthesis and mitosis.
Immunofluorescence co-staining with kinetochore marker Crest.
Chromatin immunoprecipitation (ChIP) to identify E2F4 DNA binding targets.

Main Results:

Nuclear E2F4 expression decreased during heart development, correlating with reduced cardiomyocyte proliferation.
E2F4 expression increased upon re-induction of proliferation in postnatal cardiomyocytes.
E2F4 localized to the nucleus, including kinetochores during mitosis.
E2F4 binds to centromeric alpha-satellite DNA during mitosis.
E2F4 inhibition reduced mitosis but not DNA synthesis in proliferating cardiomyocytes.

Conclusions:

E2F4 plays a necessary role in cardiomyocyte proliferation.
E2F4 is implicated in the regulation of mitosis in cardiomyocytes.