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Claudin-5 levels are reduced in human end-stage cardiomyopathy

Tessily A Mays1, Philip F Binkley, Amanda Lesinski

  • 1Department of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.

Journal of Molecular and Cellular Cardiology
|June 3, 2008
PubMed

Insights

Claudin-5, a tight junction protein, is reduced in most human cardiomyopathy patients. This finding suggests claudin-5 plays a role in heart failure development, independent of other known factors.

Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Claudin-5 is a transmembrane protein crucial for tight junctions in endothelial cells.
  • Previous research indicated claudin-5 reduction in a mouse model of cardiomyopathy.
  • Claudin-5 also localizes to cardiomyocyte lateral membranes near the extracellular matrix.

Purpose of the Study:

  • To investigate if claudin-5 levels are reduced in human cardiomyopathy.
  • To compare claudin-5 levels with other cell junction proteins in human heart failure.
  • To determine the independence of claudin-5 reduction from connexin-43 and dystrophin alterations.

Main Methods:

  • Analysis of claudin-5 and other cell junction protein levels in 62 human cardiomyopathic explant samples.
  • Comparison of protein levels between failing and non-failing heart samples.
  • Assessment of claudin-5 reduction relative to connexin-43 and dystrophin status.

Main Results:

  • Claudin-5 levels were reduced in at least 60% of human cardiomyopathy samples.
  • Claudin-5 reduction was observed independently of connexin-43 levels.
  • Reductions in other junction proteins (e.g., catenins, desmoplakin, N-cadherin) were infrequent and often co-occurred with claudin-5 or connexin-43 reduction.
  • Claudin-5 levels were reduced independently of dystrophin alterations.

Conclusions:

  • This study provides the first evidence of tight junction protein alterations in human cardiomyopathy.
  • Reduced claudin-5 is a significant finding in human heart failure.
  • Claudin-5 may be involved in novel mechanisms contributing to end-stage heart failure.

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