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Regulation of Growth Hormone Secretion and Messenger Ribonucleic Acid Accumulation in Human Somatotropinoma Cells in Vitro^*

Department of Medicine, Queen Elizabeth Hospital Edgbaston
The Department of Clinical Endocrinology, Birmingham and Midland Women’s Hospital Birmingham, United Kingdom

Address all correspondence and requests for reprints to: Dr. J. R. E. Davis, Department of Medicine, Manchester Royal Infirmary, Manchester, M13 9WL United Kingdom.

GH secretion and mRNA levels were measured in cultured cells obtained from six human pituitary somatotroph tumors to investigate their hormonal and intracellular regulation. The responses were variable between tumors, but, in general, mRNA levels were less responsive than GH release to in vitro manipulation. GH-releasing factor [GRF-(1–29) amide; 10 nM] increased GH release and mRNA levels in three of four tumors tested to 30–97% above control values, but the fourth tumor was unresponsive. Somatostatin (1 µM) inhibited GH release significantly in four of the six cases, to 35–79% of control levels, but had no inhibitory effect on GH mRNA accumulation, in contrast to earlier studies on rat pituitary tissue. Bromocriptine (100 nM) likewise inhibited GH release (50–75% of control), but not GH mRNA levels, in the four tumors tested. Forskolin (10 µM; used to activate adenylate cyclase) stimulated GH release and mRNA levels in the two cases that responded most clearly to GRF, but had no significant effect in the other tumors; however, the phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (100 nM) had no consistent effect on mRNA levels despite stimulating secretion in four of six cases. Thus, there was considerable variation in responses among the tumors tested; however, the responsiveness to GRF was approximately paralleled by that to forskolin, consistent with the suggestion that adenylate cyclase activity and responsiveness are variable among these tumors. Furthermore, the divergent effects of somatostatin on GH release and mRNA suggest uncoupling between its receptor and transcriptional regulatory mechanisms. (J Clin Endocrinol Metab 69: 704, 1989)

^* This work was supported by a grant from the Endowment Fund of the Central Birmingham Health Authority.

Received March 7, 1989.

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