Purpose:
Junctional adhesion molecules (JAMs) are a family of adhesion proteins found in tight junctions. We recently reported that JAM-A, JAM-C and coxackie-adenovirus receptor (CAR) are expressed in rabbit corneal endothelium and that antibody to JAM-A produces corneal swelling (IOVS. 2006;47:2408-2416). In this present study, we investigate JAM expression in the human corneal endothelium and retinal pigmented epithelium (RPE) and investigate the effect of JAM-A antibody on cultured RPE cell monolayers.
Methods:
Expression of JAM proteins was assessed by immunofluorescence confocal microscopy in eye bank flat mounts of human corneal endothelium, human RPE flat mounts, and cultured ARPE-19 monolayers. Dextran flux assays were performed to determine the effect of JAM-A antibody on permeability of ARPE-19 monolayers.
Results:
Expression of JAM-A, JAM-C, and CAR was observed in human corneal endothelium, and the distribution of JAM-A, JAM-C, and CAR in the corneal endothelium correlated with the tight junction marker zonula occludens-1 (ZO-1). In addition, expression of JAM-A, JAM-C and CAR was observed in intercellular junctions of ARPE-19 monolayers and human RPE tissue specimens. Lastly, ARPE-19 monolayers treated with antibody to JAM-A demonstrated a significant increase in permeability to 10,000 MW dextran with an average increase of 33%.
Conclusions:
Our results provide new evidence of JAM expression in intercellular junctions of the human corneal endothelium and retinal pigment epithelium. The observed effect of JAM-A antibody on ARPE-19 monolayer permeability is consistent with previous studies of JAM-A function and suggests JAM-A may have a role in regulation of RPE barrier function.
Keywords: cell adhesions/cell junctions • cornea: endothelium • retinal pigment epithelium