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Cardiomyocyte adhesion and hyperadhesion differentially require ERK1/2 and plakoglobin.

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Stabilizing cardiomyocyte adhesion, crucial for preventing arrhythmogenic cardiomyopathy (AC), can be achieved through various signaling pathways. These pathways enhance cell adhesion, offering new therapeutic targets for heart disease.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cell Adhesion Mechanisms

Background:

  • Arrhythmogenic cardiomyopathy (AC) is a heart disease linked to mutations in desmosomal proteins like desmoglein-2 (DSG2), plakoglobin (PG), and desmoplakin (DP).
  • Current AC therapies manage symptoms and arrhythmias, as the precise mechanisms of desmosomal proteins in cardiomyocyte function remain unclear.
  • Stabilizing desmosomal cardiomyocyte adhesion and hyperadhesion presents a novel therapeutic strategy, potentially making adhesion independent of calcium (Ca2+).

Purpose of the Study:

  • To elucidate the signaling pathways that regulate cardiomyocyte adhesion under basal and hyperadhesive conditions.
  • To investigate the role of adrenergic signaling, protein kinase C (PKC), p38 mitogen-activated protein kinase (p38MAPK), and extracellular signal-regulated kinase 1/2 (ERK1/2) in controlling cell adhesion.
  • To examine the impact of plakoglobin (PG) deficiency on these adhesion-regulating mechanisms in the context of AC.

Main Methods:

  • Utilized dissociation assays in HL-1 cells and murine ventricular cardiac slice cultures to study cardiomyocyte adhesion.
  • Investigated the effects of adrenergic signaling, PKC activation, p38MAPK inhibition, and ERK1/2 activation on cell adhesion.
  • Analyzed the recruitment of DSG2 to cell junctions and PG phosphorylation at S665.
  • Compared adhesion responses in wild-type and PG-deficient mice with an AC phenotype.

Main Results:

  • Adrenergic signaling, PKC activation, and p38MAPK inhibition enhanced cardiomyocyte adhesion (positive adhesiotropy) and induced hyperadhesion.
  • ERK1/2 activation correlated with positive adhesiotropy.
  • Adrenergic signaling promoted PG phosphorylation at S665 under both basal and hyperadhesive states.
  • Adrenergic signaling and p38MAPK inhibition led to increased DSG2 at cell junctions.
  • In PG-deficient mice, only PKC activation and p38MAPK inhibition effectively enhanced cardiomyocyte adhesion.

Conclusions:

  • Cardiomyocyte adhesion can be modulated and stabilized through distinct signaling pathways.
  • These findings highlight potential therapeutic targets for stabilizing desmosomal junctions in AC.
  • The efficacy of certain signaling mechanisms in enhancing adhesion is partially dependent on the presence of PG, as observed in AC models.