Gene Expression of Islet Cell Antigen p69 in Human, Mouse, and Rat
- Departments of Pediatrics and Immunology Ontario, Canada
- Department of Pathology, University of Toronto, The Hospital for Sick Children Toronto, Ontario, Canada
- Division of Immunogenetics, Department of Pediatrics, Rangos Research Center, Children's Hospital Pittsburgh, Pennsylvania
- Address correspondence and reprint requests to Dr. Hans-Michael Dosch, Department of Pediatrics and Immunology, The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, Canada M5G 1X8.
Based on the detection of specific antibodies and T-cell sensitization in patients with IDDM, islet cell antigen p69 (ICAp69) has been suggested to be a target antigen of diabetic autoimmunity. The biological function, tissue expression, and developmental kinetics of ICAp69 are largely unknown. We analyzed ICAp69 expression at the gene transcription and protein level in human and rodent tissues. By using template-calibrated quantitative reverse transcriptase polymerase chain reaction (RT-PCR), high levels of ICAp69 mRNA were found in human pancreatic islets and brain. In mouse and rat, ICAp69 gene expression peaked in islet cell lines followed by testis, islets, and brain. ICAp69 mRNA was found at low levels in other organs by RT-PCR but not by Northern blot analysis. In mice, ICAp69 transcription becomes detectable in fetal life, and fetal and adult gene expression patterns are similar. Western blot analysis of human and mouse tissues showed high expression of ICAp69 in brain, testis, pancreatic tissue, and islet cell lines. In these organs, ICAp69 immunoreactivity is predominately localized at the blood brain barrier (capillary endothelium), at the blood testis barrier (Sertoli cells and spermatids), and in pancreatic islets (β-cells). The subcellular localization of ICAp69 to endoplasmic reticulum, Golgi complex, and vesicles by immune electron microscopy suggests a role of this neuroendocrine molecule in cellular protein traffic and processing.
- Received April 3, 1995.
- Revision received November 30, 1995.
- Accepted November 30, 1995.
- Copyright © 1996 by the American Diabetes Association