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K. J. Mandell, L. Berglin, E. Severson, C. A. Parkos, H. F. Edelhauser; Junctional Adhesion Molecules (JAMs) in the Human Corneal Endothelium and Retinal Pigment Epithelium: Localization and Evidence for Role in Barrier Function. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3792.
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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.
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.
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%.
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.
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