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Updated: May 6, 2026

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
09:20

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

Published on: October 4, 2019

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Mena associates with Rac1 and modulates connexin 43 remodeling in cardiomyocytes

Rashmi Ram1, Andrew P Wescott, Katherine Varandas

  • 1The Heart Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio;

American Journal of Physiology. Heart and Circulatory Physiology
|November 5, 2013
PubMed

Insights

Mena protein regulates cardiac cell connections by modulating Rac1 activity and connexin 43 localization. This finding is crucial for understanding heart failure mechanisms and maintaining myocardial mechanical stability.

Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • Mena (Ena/VASP family) is an actin regulatory protein found in cardiac myocytes.
  • Its precise function at the intercalated disc (ICD) in maintaining myocardial mechanical stability is unknown.
  • We investigated Mena's role in regulating connexin 43 (Cx43) expression and localization at the ICD.

Purpose of the Study:

  • To determine Mena's role in regulating cytoskeletal organization at the cardiomyocyte ICD.
  • To elucidate Mena's interaction with the small GTPase Rac1.
  • To examine Mena's influence on connexin 43 (Cx43) expression, localization, and intercellular communication.

Main Methods:

  • Investigated Mena's association with active Rac1 in cardiomyocytes.
  • Utilized RNAi to knockdown Mena expression and assessed Rac1 activity.
  • Analyzed Cx43 expression, localization, and trafficking in Mena-knockdown cells and in mice overexpressing active Rac1.
  • Measured intercellular communication using dye transfer assays.

Main Results:

  • Mena associates with active Rac1; Mena knockdown increases Rac1 activity.
  • Mena knockdown leads to increased Cx43 expression and altered ICD localization.
  • Mena knockdown enhances intercellular communication between cardiomyocytes.
  • Rac1 overexpression increases Mena expression and causes Cx43 redistribution.

Conclusions:

  • Mena is a critical regulator of the cardiac intercalated disc (ICD).
  • Mena is required for proper Cx43 localization, partly through Rac1 regulation.
  • These findings provide insights into cytoskeletal regulation and intercellular communication in the heart.
Keywords:
Menaconnexin 43heart failure

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