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Altered thrombomodulin staining in blistering dermatoses

D E Jackson1, C A Mitchell, G Mason

  • 1Department of Medicine, Monash University, Box Hill Hospital, Vic.

Pathology
|August 1, 1996
PubMed
Summary
This summary is machine-generated.

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Thrombomodulin (TM) is lost in blistering skin diseases with acantholysis, mirroring desmoglein I (DG I) loss. This suggests TM plays a role in keratinocyte adhesion.

Area of Science:

  • Dermatology
  • Immunohistochemistry
  • Cell Biology

Background:

  • Blistering dermatoses involve keratinocyte adhesion disruption.
  • Thrombomodulin (TM) is a cell surface glycoprotein with known roles in coagulation and inflammation.
  • The role of TM in keratinocyte adhesion is not well understood.

Purpose of the Study:

  • To investigate the distribution of thrombomodulin (TM) in skin sections from patients with blistering dermatoses.
  • To correlate TM expression with desmoglein I (DG I) distribution, a key molecule in keratinocyte adhesion.

Main Methods:

  • Immunocytochemistry was used to stain skin sections.
  • Polyclonal and monoclonal anti-human TM antibodies were utilized.
  • Staining patterns were compared with those obtained using the anti-DG I antibody (32-2B).

Related Experiment Videos

Main Results:

  • A loss of TM staining was observed in acantholytic dermatoses.
  • TM loss was localized to areas of disrupted intercellular bridging between keratinocytes.
  • TM expression patterns closely paralleled DG I expression patterns.

Conclusions:

  • Thrombomodulin (TM) expression is significantly reduced in acantholytic blistering dermatoses.
  • The parallel expression of TM and DG I suggests TM is involved in keratinocyte adhesion.
  • TM may play a functional role in maintaining the integrity of the epidermal intercellular junctions.