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Corticotropin-Releasing Factor Up-Regulates Its Own Receptor Gene Expression in Corticotropic Adenoma Cells in Vitro¹

Third Division, Department of Medicine, Hirosaki University School of Medicine (Y.S., N.H., K.S., T.S.), Hirosaki 036; Department of Neurosurgery, Nagoya National Hospital (A.K.), Nagoya 460; and Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women’s Medical College (F.T., H.D.), Tokyo 162, Japan

Address all correspondence and requests for reprints to: Yoko Sakai, Third Division, Department of Medicine, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki 036, Japan.

To investigate the expression of CRF receptor (CRF-R) in human corticotropic adenoma (hCA) cells, we analyzed messenger RNA (mRNA) levels of type-1 CRF-R (CRF-R1). Adenomas were obtained from 10 patients with Cushing’s disease. Northern blot analysis using a rat CRF-R1 complementary RNA probe revealed a main hybridization band of 2.7 kilobases in all the hCAs. The CRF-R1 mRNA level significantly increased after 1 h, reached 15-fold the basal level at 8 h, and remained elevated 24 h after the addition of 10 nmol/L CRF in vitro. Dose dependency of the stimulatory effect of CRF was also demonstrated in hCA cells, whereas CRF down-regulated CRF-R1 mRNA levels in rat anterior pituitary (AP) cells. Treatment with dexamethasone or vasopressin decreased the CRF-R1 mRNA level in hCA cells, as observed in rat AP cells. In conclusion, we detected CRF-R1 mRNA in all hCAs tested. The CRF-R1 mRNA level was up-regulated by CRF itself in cultured hCA cells, in contrast to the down-regulation in rat AP cells.

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