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Endocrinology, Vol 119, 268-273, Copyright © 1986 by Endocrine Society
ARTICLES |
JA Clements, PJ Fuller, M McNally, I Nikolaidis and JW Funder
Using a rat pancreatic kallikrein cDNA probe (pcXP39), previously shown to hybridize to kallikrein mRNA in a variety of tissues, we have explored the control of kallikrein gene expression in rat anterior pituitary. Intact female rats have substantially higher levels of AP kallikrein mRNA than intact males; male levels are unaffected by castration, whereas female levels fall markedly postovariectomy. Administration of estradiol benzoate to intact male or ovariectomized female rats causes an increase in anterior pituitary levels of kallikrein mRNA. Since the pattern of responsiveness parallels that of PRL, we have studied GH3 cells grown in the presence and absence of estradiol; in neither instance was kallikrein mRNA above detection limits. Parallel changes were seen on Northern blots and by hybridization histochemistry; on emulsion autoradiography of pituitary sections, scattered positive cells were seen, but precise definition was not possible. We conclude that whereas in the submaxillary gland kallikrein gene expression appears androgen dependent and in the kidney is postulated to be mineralocorticoid regulated, in the anterior pituitary expression of the gene is under estrogen control; and that the local role(s) of pituitary kallikrein, whether precursor processing, control of blood flow, or other effects, would, in turn, appear to be modulated by estrogen in vivo.
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