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Related Concept Videos

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Anchoring junctions are multiprotein complexes that help cells connect to other cells and the extracellular matrix. Anchoring junctions are present on the lateral and basal surfaces of cells, providing strong and flexible connections. Focal adhesions are often formed due to cell interactions with the ECM substrata, which initiate signal transduction via kinase cascades and other mechanisms. Together, they provide stability and tissue integrity. There are three types of anchoring junctions:...
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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
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Tight junction defects in patients with atopic dermatitis.

Anna De Benedetto1, Nicholas M Rafaels, Laura Y McGirt

  • 1Department of Dermatology, University of Rochester Medical Center, Rochester, NY 14642, USA.

The Journal of Allergy and Clinical Immunology
|December 18, 2010
PubMed
Summary

Reduced claudin-1 in atopic dermatitis (AD) impairs skin barrier function and immune responses. Genetic variations in the CLDN1 gene are linked to AD, suggesting claudin-1 as a key factor in the condition.

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Area of Science:

  • Dermatology
  • Immunology
  • Genetics

Background:

  • Atopic dermatitis (AD) involves dry skin and immune overreactions due to epidermal barrier defects.
  • Tight junctions (TJs) below the stratum corneum control paracellular pathway permeability.

Purpose of the Study:

  • Evaluate claudin-1 expression and function in AD epithelium.
  • Identify single nucleotide polymorphisms (SNPs) in the claudin-1 gene (CLDN1) associated with AD.

Main Methods:

  • Gene expression profiling of AD and control skin epithelium.
  • Validation of intercellular proteins via tissue staining and qPCR.
  • Measurement of epithelial bioelectric properties and in vitro claudin-1 knockdown in keratinocytes.
  • Screening of CLDN1 SNPs in two independent populations.

Main Results:

  • Significantly reduced claudin-1 and claudin-23 expression in AD patients' nonlesional epithelium.
  • Impaired bioelectric barrier function in AD epidermis.
  • Claudin-1 knockdown diminished TJ function and increased keratinocyte proliferation.
  • CLDN1 SNPs associated with AD in North American populations.

Conclusions:

  • Impaired tight junctions, partly due to reduced claudin-1, contribute to barrier dysfunction in AD.
  • These findings suggest claudin-1 plays a role in AD pathogenesis and immune dysregulation.