Activity of growth hormone-releasing peptide-2 in cultured human pituitary adenoma cells and its interaction with growth hormone-releasing hormone and somatostatin

1998 ◽  
Vol 125 (2) ◽  
pp. 182-186 ◽  
Author(s):  
A. A. Bulatov ◽  
T. A. Osipova ◽  
I. S. Komolov ◽  
A. V. Martynov ◽  
C. Y. Bowers
Keyword(s):  
Growth Hormone ◽  
Pituitary Adenoma ◽  
Growth Hormone Releasing Hormone ◽  
Human Pituitary ◽  
Human Pituitary Adenoma ◽  
Releasing Hormone

Association of pituitary adenoma with neuronal christoma: A TEM study

1994 ◽  
Vol 52 ◽  
pp. 232-233
Author(s):  
Eva Horvath ◽  
Kalman Kovacs ◽  
B. W. Scheithauer ◽  
R. V. Lloyd ◽  
H. S. Smyth
Keyword(s):  
Growth Hormone ◽  
Pituitary Adenoma ◽  
Pituitary Tumor ◽  
Nervous Tissue ◽  
Alternative Explanation ◽  
Growth Hormone Releasing Hormone ◽  
Cell Hyperplasia ◽  
Releasing Hormone ◽  
Secretory Neurons

The association of a pituitary adenoma with nervous tissue consisting of neuron-like cells and neuropil is a rare abnormality. In the majority of cases, the pituitary tumor is a chromophobic adenoma, accompanied by acromegaly. Histology reveals widely variable proportions of endocrine and nervous tissue in alternating or intermingled patterns. The lesion is perceived as a composite one consisting of two histogenetically distinct parts. It has been suggested that the neuronal component, morphologically similar to secretory neurons of the hypothalamus, may initiate adenoma formation by releasing stimulatory substances. Immunoreactivity for growth hormone releasing hormone (GRH) in the neuronal component of some cases supported this view, whereas other findings such as consistent lack of growth hormone (GH) cell hyperplasia in the lesions called for alternative explanation.Fifteen tumors consisting of a pituitary adenoma and a neuronal component have been collected over a 20 yr. period. Acromegaly was present in 11 patients, was equivocal in one, and absent in 3.

scholarly journals Stimulation by Urocortin of Growth Hormone (GH) Secretion in GH-Producing Human Pituitary Adenoma Cells.

1997 ◽  
Vol 44 (4) ◽  
pp. 627-629 ◽  
Author(s):  
YOSHIO MURAKAMI ◽  
TOSHIAKI MORI ◽  
KUNIO KOSHIMURA ◽  
MASAMICHI KUROSAKI ◽  
TOMOKATSU HORI ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Pituitary Adenoma ◽  
Human Pituitary ◽  
Human Pituitary Adenoma ◽  
Gh Secretion

Cortisol inhibition of growth hormone-releasing hormone-stimulated growth hormone release from cultured sheep pituitary cells

1994 ◽  
Vol 141 (3) ◽  
pp. 517-525 ◽  
Author(s):  
J L Sartin ◽  
R J Kemppainen ◽  
E S Coleman ◽  
B Steele ◽  
J C Williams
Keyword(s):  
Growth Hormone ◽  
Cyclic Amp ◽  
Calcium Ionophore ◽  
Ionophore A23187 ◽  
Pituitary Cells ◽  
Growth Hormone Releasing Hormone ◽  
Short Term ◽  
Human Pituitary ◽  
Releasing Hormone ◽  
Short Term Culture

Abstract Cortisol inhibits growth hormone (GH) release in short-term culture and is stimulatory in long-term cultures of rat and human pituitary cells. This study sought to determine the in vitro effects of cortisol on GH release and the signal transduction pathways mediating the effects of cortisol on GH release from cultured ovine somatotrophs. Pituitary cells were dispersed with collagenase and placed in culture medium for 4 days. The data indicate that cortisol inhibited growth hormone-releasing hormone (GHRH)-stimulated GH release by at least 2 h. In short-term culture GHRH-, forskolin- and dibutyryl cyclic AMP-stimulated GH release were inhibited by cortisol, suggesting an effect distal to the membrane and involving a protein kinase A (PKA)-dependent pathway. GH release initiated by KCl was inhibited by cortisol, but GH release caused by the calcium ionophore A23187 was unaffected. This suggests a possible action of cortisol on the calcium channels. The inhibition by cortisol of the calcium-dependent secretion of GH release appeared to play a smaller role in mediating cortisol inhibition of GH release than that seen with PKA. Attempts to overcome cortisol inhibition of GH release using puromycin, arachidonic acid or pertussis toxin were unsuccessful. Since cortisol inhibition of GH release does not occur via the mechanisms found in other cell types, cortisol inhibition of pituitary cell secretions appears to be cell-specific rather than utilizing a single inhibitory mechanism. The majority of cortisol actions on the somatotroph appear to act at a site distal to the production of cyclic AMP. In contrast to man and the rat, the sheep somatotroph does not appear to increase GH release when treated with cortisol for 24 h, perhaps related to the lack of effect of cortisol on somatotroph content of GH. Journal of Endocrinology (1994) 141, 517–525

Sign in / Sign up

Export Citation Format

Share Document