Human Schlemm's canal cells express the endothelial adherens proteins, VE-cadherin and PECAM-1.

Journal Article (Journal Article)

Purpose. The majority of resistance to outflow of aqueous humor resides at or near the inner wall of Schlemm's canal (SC). Transmembrane proteins that contribute to the generation of resistance to aqueous outflow likely participate in junctional complexes between SC cells. The purpose of the present study was to examine the expression of cadherins in SC cells that play a significant role in adherens junction complexes that control permeability of vascular endothelia. Methods. Identification of cadherin subtype mRNAs was examined by hybridization screening of three different SC cDNA libraries and by polymerase chain reaction analysis with degenerate primers. Expression of endothelial adherens proteins, vascular endothelial (VE)-cadherin and platelet endothelial cell adhesion molecule-1 (PECAM-1), was examined by western blot analyses of whole cell lysates prepared from SC and trabecular meshwork cells and by immunofluorescence microscopy of frozen sections of human anterior chambers. As controls, bovine retinal, bovine aortic, human umbilical vein and human iliac vein endothelial cells were examined for VE-cadherin expression. Results. Screens of SC cDNAs revealed abundant expression of N-cadherin and VE-cadherin. Expression of VE-cadherin protein was identified in both inner and outer wall SC cells, appropriately localized to SC intercellular borders and appeared as a single band of approximately 130 kDa by western blot analysis. Specific labeling of PECAM-1 was similar to VE-cadherin and appeared as a single band of approximately 130 kDa by western blot analysis. Conclusions. VE-cadherin and PECAM-1 expression in SC suggests that SC cells are vascular in origin and contain adherens protein likely involved in restricting fluid flow across the inner wall of SC.

Full Text

Duke Authors

Cited Authors

  • Heimark, RL; Kaochar, S; Stamer, WD

Published Date

  • November 2002

Published In

Volume / Issue

  • 25 / 5

Start / End Page

  • 299 - 308

PubMed ID

  • 12658549

International Standard Serial Number (ISSN)

  • 0271-3683

Digital Object Identifier (DOI)

  • 10.1076/ceyr.


  • eng

Conference Location

  • England