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INTRODUCTION
Cytokines are soluble polypeptides released from cells of the immune system. Their production in endocrine glands and their actions on hormone-responsive cells is currently a subject of intense research interest. There is strong evidence for the involvement of cytokines in the pathogenesis of autoimmune diabetes and thyroid disease. In addition they may regulate the growth and differentiated function of cells as they are known to do in the reticuloendothelial system. Cytokines may thus contribute to the development of functional endocrine disturbances and neoplasms. They are also involved in bone modelling processes and their action may be disturbed in disorders of bone. Greater understanding of the effects of cytokines will give insight into normal regulatory processes in endocrine tissues and may lead to therapeutic advances. The aim of this article is to review these actions and to speculate as to their physiological and pathophysiological significance as well as
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Introduction
Intercellular communication is effected through the release and action of substances known as paracrine agents. Recent studies are providing increasing evidence that pituitary hormone secretion is under the control of paracrine as well as hypothalamic factors. The individual cell types within the rat anterior pituitary gland appear to be arranged in specific groups and juxtapositions, and this precise organization of cells provides an anatomical basis for an intercellular control system in the pituitary gland. There is good circumstantial evidence for a variety of paracrine interactions within the anterior pituitary gland, although the exact physiological functions of different proposed paracrine agents have yet to be fully elucidated. Many substances have been shown to affect the release of each of the pituitary hormones directly, and there is evidence that some of these are synthesized and released within the anterior pituitary and may therefore act as paracrine agents. Established and
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ABSTRACT
Gonadotrophin-releasing hormone (GnRH) stimulated the accumulation of inositol phosphates and prolactin secretion in anterior pituitary cells from young male rats. Saralasin ([Sar1,Ala8]-angiotensin II; a competitive antagonist of angiotensin II) inhibited the increase in both inositol phosphates and prolactin in a dose-dependent manner. Since angiotensin II has been shown to be a potent stimulus for inositol phosphate accumulation and prolactin secretion in the lactotroph, these findings suggest that angiotensin II acts as a paracrine agent, being released from the gonadotroph in response to GnRH and causing the lactotroph to release prolactin through an effect on phosphoinositide metabolism. The ability of GnRH to promote prolactin release was lost in pituitaries from older rats, and the increase in total inositol phosphate accumulation was less. These findings provide evidence of a physiological role for the presence of the renin–angiotensin system within the pituitary gland.
J. Endocr. (1988) 116, 367–371
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SUMMARY
As part of a continuing study of adrenal steroids in relation to breast cancer, various experiments were performed in order to study relationships between androgen and corticosteroid biosynthesis. Chopped tumour tissue from a 'mixed cell' adrenal adenoma (7·4 g.) removed from a patient in Cardiff Royal Infirmary was incubated with [4-14C]pregnenolone and [7α3H]17α-hydroxypregnenolone for periods of time ranging from 30 to 120 min. The results of this work suggest that 17α-hydroxyprogesterone may not be an obligatory intermediate in androgen or cortisol synthesis. Evidence from further experiments with 'normal' human adrenal tissue removed from breast cancer patients using previously established ultramicrochemical techniques indicates that dehydroepiandrosterone (DHA) sulphokinase enzyme system is confined to the zona reticularis of the gland. The conversion of [7α-3H]DHA sulphate, [7α-3H]androstenedione and [7α-3H]testosterone to oestrogens and their conjugates by adrenal homogenates was also investigated. Conversions were extremely low from all precursors.
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Pharmacology Division, National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-ku, Tokyo 104, Japan and *Department of Zoology and Cancer Research Laboratory, University of California, Berkeley, California 94720, U.S.A.
(Received 24 April 1978)
Recent studies have demonstrated that neonatal exposure of female mice to oestradiol-17β, testosterone, diethylstilboestrol and 5β-dihydrotestosterone results in increased plasma levels of prolactin in animals as old as 15 months (Yanai, Mori & Nagasawa, 1977; Nagasawa, Mori, Yanai, Bern & Mills, 1978). Treatment with these hormones (Mori, Bern, Mills & Young, 1976; Jones & Bern, 1977; Nagawasa et al. 1978) or with progesterone (Jones & Bern, 1977; Jones, Bern & Wong, 1977) also results in normal and neoplastic stimulation of the mammary gland, which is dependent on the presence of the ovaries. The present communication provides data on plasma levels of prolactin in old female mice treated neonatally with oestradiol or progesterone or both steroids and the effects
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ABSTRACT
Immunoreactive tissue kallikrein was co-localized with prolactin in all the eleven prolactin-secreting adenomas of the human anterior pituitary gland examined in this study. The intracellular distribution of immunoreactivity in the prolactin-secreting cells suggests that tissue kallikrein is located within the Golgi complex of these cells. Both the intracellular hormone-processing action and the kininogenase activity of tissue kallikrein may be of functional importance in human prolactinomas.
Journal of Endocrinology (1990) 124, 327–331
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ABSTRACT
Interleukin-6 (IL-6) has actions on a variety of endocrine tissues. The cytokine is secreted by cells of the anterior pituitary and endocrine pancreas and has recently been shown to be produced by cultures of thyroid epithelial cells. In this study we have examined some of the factors which regulate IL-6 release from an immortalized human thyroid line (HTori3).
IL-6 release over 24 h was stimulated by TSH (5000 μU/ml), by forskolin (0·01 mmol/l), by fetal calf serum (1–20%) and by epidermal growth factor (20 ng/ml). Stimulation was also apparent with γ-interferon and with tumour necrosis factor at concentrations known to enhance class II major histocompatibility antigen expression by thyroid epithelium. The most potent factor tested was interleukin-1 (IL-1), which controls IL-6 release from other cell types. Threefold stimulation was found with 1 U/ml rising to 350-fold with 1000 U/ml. The effect of IL-1 took 2 h to develop and was blocked by cycloheximide (100 μmol/l). Stimulation was not markedly inhibited by pertussis toxin. Many of the actions of IL-1 are mediated by prostaglandin E2 (PGE2). At concentrations as low as 30 nmol/l, PGE2 stimulated IL-6 release but the maximum stimulation obtained with PGE2 was only threefold. The effect of IL-1 was not inhibited by indomethacin.
These data provide further evidence that IL-6 is produced by human thyrocytes. The effect of IL-1 has not been demonstrated previously. Stimulation of IL-6 release by IL-1 did not appear to be mediated by prostaglandin. IL-6 may influence hormone release from the thyroid as it does in other tissues. High concentrations of IL-6 in the thyroid may increase infiltration by, and activation of, lymphocytes in patients with autoimmune thyroid disease.
Journal of Endocrinology (1992) 133, 477–482
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Mammogenesis in primiparous hypophysectomized goats has been assessed between days 60 and 120 of gestation and compared with that found in untreated goats and goats treated with 5 mg bromocriptine/day. There were fivefold increases in the weight of lobulo-alveolar tissue in the hypophysectomized and bromocriptine-treated goats and a tenfold increase in the untreated goats. Histological examination of the mammary glands at 120 days showed normal structure, and determinations of lactose, lactose synthetase, cytosol enzymes, protein, DNA and RNA indicated qualitatively normal initiation of milk synthetic capabilities in both the hypophysectomized and bromocriptine-treated goats. Bromocriptine treatment lowered the plasma concentration of placental lactogen as well as that of prolactin.
The results indicate that placental lactogen has important mammogenic effects during pregnancy.
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ABSTRACT
Tissue kallikrein is a serine protease which may be involved in the intracellular processing of prolactin in the anterior pituitary gland. The expression of tissue kallikrein, in the rat, is promoted by oestrogen and inhibited by dopamine. Human and rat prolactinomas contain markedly increased amounts of tissue kallikrein; this is comparatively reduced if patients are pretreated with the dopamine agonist, bromocriptine, before surgery. Some GH-secreting adenomas are mixed and also contain prolactin-secreting cells. We therefore investigated 27 GH-immunostaining human pituitary adenomas for the presence of immunoreactive tissue kallikrein. Sixteen of the adenomas had positive immunostaining for prolactin; eight of these patients had associated clinical hyperprolactinaemia before the tumour was removed. Tissue kallikrein immunoreactivity was found in ten adenomas, all of which also had prolactin immunopositivity. There was a close relationship between the percentage of cells staining for prolactin and tissue kallikrein but not for GH. A further eight adenomas had patchy positivity, i.e. less than 1% of cells immunostained for tissue kallikrein and six of these also had some prolactin-staining cells. Nine out of eleven purely GH-staining adenomas had no tissue kallikrein immunopositivity, the remaining two showing patchy staining. A review of bromocriptine responsiveness, as assessed by mean GH hormone levels during oral glucose tolerance tests before and after therapy was commenced, indicated that patients with adenomas which stained for prolactin and tissue kallikrein were more likely to respond to bromocriptine than those which failed to do so.
Journal of Endocrinology (1992) 134, 149–154
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ABSTRACT
Analysis of ovine conceptus RNA by slot blotting, Northern analysis and nested polymerase chain reaction failed to detect oxytocin–neurophysin prohormone mRNA. Probes used hybridized with both the 3' end of the prohormone mRNA and the oxytocin-coding sequence. Northern analysis of bovine and porcine conceptus RNA was also negative, and polymerase chain reaction demonstrated oxytocin–neurophysin mRNA in ovine corpus luteum, but not in human corpus luteum or decidua, or in ovine endometrium. Infusion of oxytocin into the uterine lumen in cyclic ewes between days 9 and 19 or 20 after oestrus failed to prolong the luteal phase of the cycle and had no effect on endometrial oxytocin receptor concentrations or uterine prostaglandin F secretion. Oxytocin administered systematically prevented luteolysis and reduced uterine prostaglandin F secretion. Taken together, these data suggest that blastocyst-derived oxytocin is unlikely to contribute to corpus luteum maintenance in early pregnancy. They are inconsistent with a previous report that the ovine blastocyst synthesizes and secretes oxytocin.
Journal of Endocrinology (1991) 130, 443–449
