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₁ Connexin 43 Gap Junctions Are Decreased in Human Adrenocortical Tumors¹

Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine (S.A.M., K.D.), Pittsburgh, Pennsylvania 15261; the Medical Research Service, Veterans Affairs Medical Center and Division of Endocrinology, Department of Medicine, University of Miami School of Medicine (L.M.F.), Miami, Florida 33125; and the Department of Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health (S.R.B.), Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: Dr. Sandra A. Murray, Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261.

Gap junctional communication disorders have been implicated in the etiology of benign and malignant tumors. Understanding the type, distribution, and frequency of gap junctions in adrenal disorders should provide insight into the role of gap junctions in adrenal carcinogenesis as well as information that may be useful in developing improved diagnosis and treatment of adrenal diseases. Using immunocytochemical techniques, we have characterized and compared ₁ connexins 43 gap junction protein levels in normal adrenal glands to those in benign and malignant adrenocortical human tumors. In addition, gap junction protein levels were studied in a human adrenal cancer cell line (H295). In both normal and neoplastic adrenal tissues, only ₁ connexin 43 could be detected, whereas ß₁ connexin 32 and ß₂ connexin 26 were not found. In the normal adrenal gland, the zona fasciculata was demonstrated to have the highest number of gap junctions per cell (mean ± SEM, 13.78 ± 1.93). In contrast, in benign adrenocortical adenomas, the number of gap junctions per cell compared to that detected in normal adrenal glands was significantly reduced (mean ± SEM, 4.6 ± 1.17; P 0.05), and the lowest number was found in malignant adrenocortical tumors (1.42 ± 0.58; P 0.05). Similarly, there were few or no ₁ connexin 43 gap junctions in the H295 population. There was a progressive decrease in gap junction plaques in adrenocortical cancer cell populations compared to those in normal cell populations. Therefore, analysis of gap junction protein may be helpful for the differential diagnosis of benign and malignant adrenal tumors. The induction of gap junctions in malignant cells may provide a novel therapeutic strategy for adrenal cancer.

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