期刊
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
卷 48, 期 9, 页码 3928-3936出版社
ASSOC RESEARCH VISION OPHTHALMOLOGY INC
DOI: 10.1167/iovs.06-1536
关键词
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资金
- NEI NIH HHS [P30 EY006360, P30EY006360, P30 EY006360-20, R01 EY000933, R01 EY000933-35] Funding Source: Medline
- NIDDK NIH HHS [R01 DK72564, R01 DK061379, R01 DK061379-06, R01 DK072564, R01 DK072564-13] Funding Source: Medline
- NIGMS NIH HHS [T32 GM008169] Funding Source: Medline
PURPOSE. Junctional adhesion molecules (JAMs) are a family of adhesion proteins found in intercellular junctions. Evidence suggests that JAM-A is important for the regulation of tight junction assembly and epithelial barrier function. The authors recently reported that JAM- A is expressed in rabbit corneal endothelium and that antibody to JAM- A produces corneal swelling. In the present study, they investigate JAM-A expression in the human corneal endothelium and retinal pigment epithelium (RPE) and examine the effect of a function-blocking antibody to JAM- A on the permeability of cultured RPE cell monolayers. METHODS. Expression of JAM- A in human corneal endothelium, human RPE tissue, and cultured ARPE-19 monolayers was assessed by immunofluorescence confocal microscopy. Localization of JAM- A was compared with the tight junction-associated protein zonula occludens-1 (ZO-1). To investigate JAM- A function in ARPE-19 cells, ARPE-19 monolayers were subjected to a calcium switch protocol to disrupt cell junctions and treated with a function-blocking antibody to JAM- A or an isotype-matched control. Dextran flux assays were performed to assess the effect of JAM- A antibody on ARPE-19 monolayer permeability. RESULTS. Expression of JAM- A was observed in human corneal endothelium, and its distribution correlated with the tight junction-associated protein ZO-1. In addition, expression of JAM- A was observed in human RPE and in intercellular junctions of ARPE-19 monolayers. The localization pattern of JAM- A in the RPE and ARPE-19 monolayers was similar to that of ZO-1. ARPE-19 monolayers treated with antibody to JAM- A demonstrated a 33% increase in permeability to 10,000 MWt dextran compared with monolayers treated with control antibody. CONCLUSIONS. Results of this study provide new information about JAM- A expression in tight junctions of the human corneal endothelium and human RPE. The observation that antibodies to JAM- A increase ARPE-19 monolayer permeability is consistent with previous findings of JAM- A function in epithelial tight junctions and suggests JAM-A may have a role in the regulation of RPE barrier function.
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