Full Papers
N-Cadherin Involvement in Cardiac Myocyte Interaction and Myofibrillogenesis

https://doi.org/10.1006/dbio.1994.1062Get rights and content

Abstract

N-cadherin is a cell-surface, Ca2+-dependent adhesion molecule found in intercalated disks and extrajunctional sites in the myocardium. In this paper we show that antibodies specific for N-cadherin inhibit the contraction of both interacting and single myocytes isolated from embryonic chicken hearts. Quantitative electron microscopy revealed that anti-N-cadherin significantly decreases cell-cell contact between interacting myocytes, consistent with a role for N-cadherin as a cell-cell adhesion molecule. In addition, quantitative electron microscopy showed that anti-N-cadherin treatment of cardiomyocytes results in a significant reduction in the cytoplasmic area occupied by myofibrils, implying that N-cadherin also plays a role in myofibrillogenesis. We propose that N-cadherin, in addition to mediating cardiac myocyte interaction, promotes myofibril formation necessary for functional activity of the myocardium.

References (0)

Cited by (89)

  • N-Cadherin is a prospective cell surface marker of human mesenchymal stem cells that have high ability for cardiomyocyte differentiation

    2013, Biochemical and Biophysical Research Communications
    Citation Excerpt :

    N-Cadherin is localized in the cell–cell contacts of cardiomyocytes and plays essential roles for formation of the cardiac intercalated disk structure that electromechanically couples adjacent cardiac myocytes. Addition of antibodies against N-cadherin to the cultured cardiomyocytes [20], mesodermal explants [21] or injected into embryos [22] caused a reduction in the number of myofibrils and destroy stress fibers [23]. In primary cardiomyocytes dissociated from adult rat heart, N-cadherin diffusely distributed around the cell periphery begins to co-localize with desmocollin, plakoglobin, and plakophilin-2 at the cell contact sites.

  • N-Cadherin-mediated adhesion and signaling from development to disease: Lessons from mice

    2013, Progress in Molecular Biology and Translational Science
    Citation Excerpt :

    As earlier studies demonstrated the importance of N-cadherin for myofibril formation and maintenance, this result was not expected. These former studies employed function-blocking antibodies33,34 or dominant-negative cadherin molecules35 to perturb N-cadherin function in cultured cardiomyocytes. The discrepancy in these results may be explained by the different experimental approaches.

  • Neuronal cadherin (NCAD) increases sensory neurite formation and outgrowth on astrocytes

    2012, Neuroscience Letters
    Citation Excerpt :

    Function blocking antibodies, however, may have unintended effects, including binding to other molecules and/or steric hindrance. Genetic deletion of the corresponding molecule transcends these limitations, and has both confirmed and repudiated prior blocking antibody studies that implicated NCAD in various cellular interactions [8,32,51]. Because mice lacking NCAD have many developmental defects and die embryonically [45], we have developed an in vitro neurite outgrowth assay after deleting NCAD from astrocytes cultured from Ncadflox/flox mice with an adeno-associated virus (AAV) that expresses Cre recombinase.

  • Dysregulation of cadherins in the intercalated disc of the spontaneously hypertensive stroke-prone rat

    2010, Journal of Molecular and Cellular Cardiology
    Citation Excerpt :

    The reorganisation of homophilic cell–cell adhesion is mainly regulated by the cadherin/catenin system, which is differentially modulated to sustain cell structural rather than signalling needs. N-cadherin, which is normally expressed in the adult heart is required for maintenance of the structural integrity and myofibril continuity across the plasma membrane [27,28]. In the SHRSP model, levels of N-cadherin appeared to be relatively unaltered compared to controls.

View all citing articles on Scopus
View full text