Expression and distribution of junctional adhesion molecule-1 in the human cornea

Lizhong Chen1, Nobuyuki Ebihara, Keiko Fujiki

  • 1Department of Ophthalmology, Second Affiliated Hospital of China Medical University, Shenyang, China.

Insights

Junctional adhesion molecule 1 (JAM-1) is expressed in human corneal epithelial and endothelial cells but not keratocytes. Its expression can be induced in corneal myofibroblasts, impacting corneal tissue structure.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Biology

Background:

  • Junctional adhesion molecule 1 (JAM-1) plays a role in cell-cell adhesion and epithelial barrier function.
  • Understanding JAM-1 expression in corneal cells is crucial for comprehending corneal tissue integrity.

Purpose of the Study:

  • To investigate the expression and distribution of junctional adhesion molecule 1 (JAM-1) in human corneal tissue and cells.
  • To determine if JAM-1 is present in corneal epithelial cells, endothelial cells, and keratocytes.

Main Methods:

  • Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect JAM-1, ZO-1, and occludin mRNA expression.
  • Flow cytometry (FACS) analyzed JAM-1 protein presence in cultured corneal cells.
  • Double immunofluorescence staining examined JAM-1 and occludin tissue distribution in human corneas.

Main Results:

  • Strong mRNA expression of JAM-1, ZO-1, and occludin was found in corneal epithelial and endothelial cells, but not keratocytes.
  • JAM-1 protein was confirmed in cultured epithelial and endothelial cells via FACS.
  • JAM-1 was detected in corneal myofibroblasts upon differentiation from keratocytes, and localized to cell borders in the epithelium and cytoplasm in endothelial cells.

Conclusions:

  • JAM-1 is expressed by human corneal epithelial and endothelial cells.
  • Keratocytes do not express JAM-1, but its expression is induced in corneal myofibroblasts.
  • JAM-1's presence in specific corneal cell types suggests a role in maintaining corneal barrier function.
Abstract

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