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Differential Regulation of ENA-78 and GCP-2 Gene Expression in Human Corneal Keratocytes and Epithelial Cells

From the Department of Microbiology and Immunology, College of Medicine, University of South Alabama, Mobile, Alabama.

PURPOSE. To determine whether interleukin (IL)-1- and tumor necrosis factor (TNF)-–stimulated human corneal epithelial cells (HCECs) and human corneal keratocytes (HCKs) produce the -chemokines epithelial cell-derived neutrophil attractant (ENA)-78 and granulocyte chemotactic protein (GCP)-2.

METHODS. Cultures of HCECs and HCKs were stimulated with either human recombinant IL-1 or TNF-. At selected times after stimulation, culture supernatants were harvested and assayed for ENA-78 and GCP-2 by enzyme-linked immunosorbent assay. RNA was extracted from cell cultures to measure steady state levels of intracellular ENA-78 and GCP-2 pre-mRNA and mRNA by the reverse transcription–polymerase chain reaction.

RESULTS. Exposure of HCECs to either IL-1 or TNF- stimulated a more than 4.5-fold increase in ENA-78 RNA and protein synthesis without stimulating a significant increase in either GCP-2 RNA synthesis or protein production. Exposure of HCK to IL-1 stimulated a 10-fold increase in ENA-78 and GCP-2 RNA synthesis and a more than 300-fold increase in ENA-78 and GCP-2 protein production. In contrast, exposure of keratocytes to TNF- significantly enhanced ENA-78 RNA synthesis, resulting in a more than 68-fold increase in ENA-78 protein synthesis without significantly enhancing either GCP-2 gene expression or protein secretion.

CONCLUSIONS. ENA-78 gene expression is significantly enhanced in both HCECs and HCKs in response to either IL-1 or TNF- stimulation. In contrast, GCP-2 synthesis is only inducible in IL-1–stimulated HCKs. The results suggest that GCP-2 gene expression is more tightly regulated in diseased or injured corneal tissue than is ENA-78 gene expression.

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