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.
Synthesis and secretion of POMC-derived peptides appear to be differentially regulated in the anterior pituitary (AP) and neurointermediate lobe (NIL). In the AP, glucocorticoids inhibit, and CRF and arginine vasopressin stimulate, synthesis of POMC and release of immunoreactive (ir)-beta-endorphin (beta EP); in the NIL, synthesis and release of POMC and its derivatives are under tonic inhibitory dopaminergic control. There is, however, evidence for some overlap of these control mechanisms under certain circumstances. In the present study we have used specific RIA and Northern blot analysis to examine the effects of chronic treatment with dopaminergic agents and dexamethasone (DM) (both alone and in combination) on AP and NIL content of ir-beta EP and POMC messenger RNA (mRNA), and/or hypothalamic ir-arginine vasopressin and ir-CRF content. In the NIL, the dopamine agonist bromocriptine reduced and the antagonist haloperidol raised both POMC mRNA and ir-beta EP content. Long term DM treatment did not alter NIL ir-beta EP content in the intact rat, but increased levels of POMC mRNA. DM abolished the haloperidol-induced increase in NIL ir-beta EP content but further increased the haloperidol-induced rise in POMC mRNA. DM treatment lowered both ir-beta EP and POMC mRNA in the AP as well as lowering levels of hypothalamic ir-CRF. In DM-treated rats, haloperidol partially restored AP ir-beta EP and POMC mRNA to control untreated levels. These findings further support the proposition that both dopaminergic agents and glucocorticoids can modulate POMC mRNA levels and/or tissue content of ir-beta EP in both the NIL and AP of the rat. The effects of DM on the NIL, both alone or with haloperidol, suggest that glucocorticoids may have both direct and indirect effects on POMC gene expression in this tissue.
The neurohypophysial hormones oxytocin and arginine vasopressin (AVP) have been identified on immunological criteria in the ovary. Confirmation of extraneuronal synthesis requires the demonstration in the tissue of the specific messenger RNA (mRNA) for the preprohormone. Using a synthetic pentadecamer nucleotide probe, highly specific for the 5' region of rat neurophysin II (NP II), we have demonstrated the presence of AVP-NP II mRNA in the ovary of Sprague-Dawley, Long-Evans and Brattleboro rats, with an apparent molecular weight identical to that seen for hypothalamus. These findings, together with the presence of immunoreactive AVP in the ovaries but not hypothalami of Brattleboro rats, suggest that tissue-specific differences in AVP-NP II gene expression occur at the translational as well as transcriptional level.
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