N-cadherin/catenin complex as a master regulator of intercalated disc function.

Cell Commun Adhes

Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA , USA.

Published: June 2014

Intercellular adhesive junctions are essential for maintaining the physical integrity of tissues; this is particularly true for the heart that is under constant mechanical load. The correct functionality of the heart is dependent on the electrical and mechanical coordination of its constituent cardiomyocytes. The intercalated disc (ID) structure located at the termini of the rod-shaped adult cardiomyocyte contains various junctional proteins responsible for the integration of structural information and cell-cell communication. According to the classical description, the ID consists of three distinct junctional complexes: adherens junction (AJ), desmosome (Des), and gap junction (GJ) that work together to mediate mechanical and electrical coupling of cardiomyocytes. However, recent morphological and molecular studies indicate that AJ and Des components are capable of mixing together resulting in a "hybrid adhering junction" or "area composita." This review summarizes recent progress in understanding the in vivo function(s) of AJ components in cardiac homeostasis and disease.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6054126PMC
http://dx.doi.org/10.3109/15419061.2014.908853DOI Listing

Publication Analysis

Top Keywords

intercalated disc
8
n-cadherin/catenin complex
4
complex master
4
master regulator
4
regulator intercalated
4
disc function
4
function intercellular
4
intercellular adhesive
4
adhesive junctions
4
junctions essential
4

Similar Publications

Cell-cell junctions in focus - imaging junctional architectures and dynamics at high resolution.

J Cell Sci

October 2024

Amsterdam UMC, University of Amsterdam, Department of Medical Biochemistry, Amsterdam Cardiovascular Sciences, 1105 AZ, Amsterdam, The Netherlands.

Studies utilizing electron microscopy and live fluorescence microscopy have significantly enhanced our understanding of the molecular mechanisms that regulate junctional dynamics during homeostasis, development and disease. To fully grasp the enormous complexity of cell-cell adhesions, it is crucial to study the nanoscale architectures of tight junctions, adherens junctions and desmosomes. It is important to integrate these junctional architectures with the membrane morphology and cellular topography in which the junctions are embedded.

View Article and Find Full Text PDF
Article Synopsis
  • Becker muscular dystrophy (BMD) is a less severe X-linked genetic disorder caused by mutations in the DMD gene, resulting in truncated dystrophin and affecting muscle function, particularly in the heart.
  • Researchers created a rat model for BMD by deleting specific exons of the Dmd gene and evaluated the rats for functional and histopathological changes during their first year, finding moderate muscle damage and progressive heart disease.
  • RNA sequencing of cardiac tissue revealed shared abnormalities in BMD and Duchenne muscular dystrophy (DMD) rats, pointing to issues with key proteins at cell junctions, which could help understand dystrophin's role in muscle and heart function, and pave the way for new treatments.
View Article and Find Full Text PDF

Caveolin is a monotopic integral membrane protein, widely expressed in metazoa and responsible for constructing enigmatic membrane invaginations known as caveolae. Recently, the high-resolution structure of a purified human caveolin assembly, the CAV1-8S complex, revealed a unique organization of 11 protomers arranged in a tightly packed, radially symmetric spiral disc. One face and the outer rim of this disc are highly hydrophobic, suggesting that the complex incorporates into membranes by displacing hundreds of lipids from one leaflet.

View Article and Find Full Text PDF

Background: A structural heart disease or functional electrical abnormalities can cause an electrical storm.

Case Presentation: We present a young boy with an electrical storm who had no cardiac risk factors and a positive family history of sudden cardiac death. The stepwise diagnostic approach was ineffective in determining previously known causes as the origin of the electrical storm.

View Article and Find Full Text PDF

Background: Cardiac arrhythmias are the main cause of sudden death due to Chronic Chagasic Cardiomyopathy (CCC). Here we investigated alterations in connexin 43 (Cx43) expression and phosphorylation in cardiomyocytes as well as associations with cardiac arrhythmias in CCC.

Methods: C57Bl/6 mice infected with underwent cardiac evaluations at 6 and 12 months after infection via treadmill testing and EKG.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!