Tissue factor expression in human pterygium

Mol Vis. 2011 Jan 8:17:63-9.

Abstract

Purpose: A pterygium shows tumor-like characteristics, such as proliferation, invasion, and epithelial-mesenchymal transition (EMT). Previous reports suggest that tissue factor (TF) expression is closely related to the EMT of tumor cells, and subsequent tumor development. In this study, we analyzed the expression and immunolocalization of TF in pterygial and normal conjunctival tissues of humans.

Methods: Eight pterygia and three normal bulbar conjunctivas, surgically removed, were used in this study. Formalin-fixed, paraffin-embedded tissues were submitted for immunohistochemical analysis with anti-TF antibody. Double staining immunohistochemistry was performed to assess TF and alpha-smooth muscle actin (α-SMA) or epidermal growth factor receptor (EGFR) expression in the pterygia.

Results: Immunoreactivity for TF was detected in all pterygial tissues examined. TF immunoreactivity was localized in the cytoplasm of basal, suprabasal, and superficial epithelial cells. The number of TF-immunopositive cells in pterygial epithelial cells was significantly higher than in normal conjunctival epithelial cells (p<0.001). TF immunoreactivity was detected in α-SMA-positive or -negative pterygial epithelial cells. EGFR immunoreactivity was detected in pterygial epithelium, which was colocalized with TF.

Conclusions: These results suggest that TF plays a potential role in the pathogenesis and development of a pterygium, and that TF expression might be involved through EMT-dependent and -independent pathways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / biosynthesis
  • Conjunctiva / metabolism
  • Cytoplasm / metabolism
  • Epithelial Cells / metabolism
  • Epithelium / pathology
  • ErbB Receptors / biosynthesis
  • Formaldehyde / pharmacology
  • Gene Expression Regulation*
  • Humans
  • Immunohistochemistry / methods
  • Mesoderm / pathology
  • Models, Biological
  • Pterygium / metabolism*
  • Signal Transduction
  • Thromboplastin / biosynthesis*

Substances

  • Actins
  • Formaldehyde
  • Thromboplastin
  • ErbB Receptors