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(Investigative Ophthalmology and Visual Science. 2004;45:4284-4292.)
© 2004 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.03-1052
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Modulation of Corneal Epithelial Cell Functions by the Neutrophil-Derived Inflammatory Mediator CAP37

H. Anne Pereira,1 Xin Ruan,1 Melva L. Gonzalez,1 Irina Tsyshevskaya-Hoover,1 and James Chodosh2

1From the Departments of Pathology and 2Ophthalmology, University of Oklahoma Health Sciences Center, Dean A. McGee Eye Institute, Oklahoma City, Oklahoma.

PURPOSE. To investigate the effect of CAP37, an inflammatory mediator in neutrophils, on three important events in corneal wound healing: proliferation, migration, and adhesion.

METHODS. Immortalized human corneal epithelial cells (HCEC) were treated with CAP37, and its effects on migration and proliferation were measured using the modified Boyden chemotaxis chamber and the proliferation assays (CyQUANT; Molecular Probes, Eugene, OR), respectively. Effects on adhesion were determined by measuring upregulation of adhesion molecules belonging to the selectin, integrin, and immunoglobulin superfamily using RT-PCR and flow cytometry.

RESULTS. CAP37 promoted proliferation of HCEC in a time- and dose-dependent fashion. CAP37 was maximally chemotactic for HCEC over a range of 1.3 x 10–8 to 5.2 x 10–8 M. CAP37 upregulated intercellular adhesion molecule (ICAM)-1, platelet endothelial cell adhesion molecule (PECAM)-1, and integrin molecules {alpha}3 (CD49c) and ß1 (CD29). Data on migration and ICAM-1 and PECAM-1 upregulation were corroborated using primary human corneal epithelial cells.

CONCLUSIONS. CAP37 modulated corneal epithelial cell proliferation and migration and upregulated adhesion molecules involved in leukocyte–epithelial and epithelial–extracellular matrix interactions.




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