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Expression of Chromogranin-A Messenger Ribonucleic Acid in Parathyroid Tissue from Patients with Primary Hyperparathyroidism^*

MICHAEL A. LEVINE, MICHAEL A. DEMPSEY, LEE J. HELMAN and THOMAS G. AHN

Division of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, (M.A.L., M.A.D., T.G.A.) Baltimore, Maryland 21205
the Molecular Genetics Section, Pediatric Branch, National Cancer Institute (L.J.H.) Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: Dr. Michael A. Levine, Division of Endocrinology and Metabolism, Hunterian Building, Room 816, 725 North Wolfe Street, Baltimore, Maryland 21205.

Chromogranin-A (CgA), also termed secretory protein-I, is an acidic glycoprotein that is synthesized and secreted by cells of the diffuse endocrine and neuroendocrine system. Several previous studies had suggested that plasma levels of CgA were elevated in patients with primary hyperparathyroidism. In the present study we sought to examine expression of the CgA gene in human parathyroid tissue from patients with primary hyperparathyroidism. We characterized the mRNAs coding for CgA and β-actin in parathyroid tissue fragments obtained from 12 patients with parathyroid adenomas, 11 patients with familial multiple endocrine neoplasia type I (FMEN I) with parathyroid hyperplasia, and 11 normal subjects. The mRNAs were detected and analyzed by dot and Northern blot hybridization using cDNA probes. CgA mRNA transcripts of 2.1 kilobases were detected in normal and pathological parathyroids. Similarly, β-actin mRNA species of 2.1 kilobases was present in all tissues. The relative level of parathyroid tissue CgA mRNA, calculated as the CgA/β-actin mRNA ratio, was 73 ± 18 in parathyroid adenoma, 73 ± 20 in FMEN I, and 100 ± 9 in controls (mean ± SE; expressed as a percentage of the control reference group value). There were no significant differences among the steady state levels of CgA mRNA levels in these three groups (F = 0.98; P = 0.39). These results demonstrate that expression of CgA mRNA is qualitatively and quantitatively normal in parathyroid tumors from patients with FMEN I and parathyroid adenoma.

^* Presented in part at the Ninth Annual Meeting of the American Society for Bone and Mineral Research, Indianapolis, IN 1987. This work was supported in part by NIH Grant DK-38990, the Clinical Research Center at the Johns Hopkins University, supported by NIH Grant RR-00035, and a Johns Hopkins University Institutional grant.

Recipient of a National Research Service Award (AM-07898) from the NIH.

Received December 6, 1989.

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