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Early-Life Stress Regulates Cardiac Development through an IL-4-Glucocorticoid Signaling Balance.

Dilem C Apaydin1, Paul A Morocho Jaramillo1, Laura Corradi1

  • 1Max Delbrück Center for Molecular Medicine, Robert-Rössle-Straße 10, 13092 Berlin, Germany.

Cell Reports
|November 18, 2020
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Summary

Early life stress disrupts heart development by reducing cardiomyocyte cell division via the glucocorticoid receptor (GR). This stress pathway interacts with interleukin-4 (IL-4) signaling, impacting cardiac growth and function.

Keywords:
Stat3cardiomyocytecytokineglucocorticoidheart developmentinterleukin-4stresszebrafish

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Area of Science:

  • Cardiovascular Science
  • Developmental Biology
  • Neuroendocrinology

Background:

  • Early life stress is a known risk factor for adult cardiovascular diseases.
  • The precise mechanisms by which stress influences the susceptibility to cardiovascular disease onset are not fully understood.
  • Understanding how stress impacts cardiac development is crucial for preventing long-term health consequences.

Purpose of the Study:

  • To investigate how early life stress affects myocardial growth and cardiomyocyte proliferation.
  • To elucidate the molecular pathways involved in stress-induced cardiac developmental disruption.
  • To identify the interplay between stress response and immune signaling in cardiac development.

Main Methods:

  • Analysis of myocardial growth and cardiomyocyte mitotic activity following exposure to stress.
  • Investigation of the role of the glucocorticoid receptor (GR) in cardiac development.
  • Examination of the interaction between GR signaling and interleukin-4 (IL-4) pathways, including signal transducer and activator of transcription 3 (Stat3).

Main Results:

  • Brain-processed stress significantly reduces cardiomyocyte mitotic activity, disrupting myocardial growth.
  • Activation of the glucocorticoid receptor (GR) impairs cardiomyocyte numbers, trabecular formation, and cardiac contractility.
  • An antagonistic interaction between GR and interleukin-4 (IL-4) signaling was identified, with IL-4 promoting cell-cycle progression and GR inhibiting it.

Conclusions:

  • Early life stress, mediated by GR activation, negatively impacts developing heart structure and function.
  • A critical interplay exists between stress (GR) and immune (IL-4/Stat3) signaling pathways in regulating cardiomyocyte cell division.
  • These findings reveal a novel mechanism linking stress, immune modulation, and cardiac development, offering potential targets for cardiovascular disease prevention.