bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neurotransmitters and lymphatic-vascular transfer of prostaglandin F2α stimulate ovarian oxytocin output in sheep
Authors: Heap R. B. , Fleet I. R. , Davis A. J. , Goode J. A. , Hamon M. H. , Walters D. E. , Flint A. P. F. 
Published: December 2008

ABSTRACT
The mechanisms of lymphatic-vascular transfer across the ovarian vascular pedicle were studied in anaesthetized sheep 8–15 days after ovulation. [3H]Prostaglandin F2α (PGF2α), [14C]mannitol and [36Cl]Na were infused continuously into either a uterine lymphatic or a uterine vein and the kinetics of transfer into the adjacent utero-ovarian vein or ovarian plasma were studied. Transfer occurred according to the sequence [36Cl] > [14C] > [3H] indicating that PGF2α is not transferred by rapid diffusion, as with [36Cl]Na, nor by a paracellular route, as with [14C]mannitol, but by a slower process probably involving facilitated diffusion.
Transfer into the adjacent utero-ovarian vein or ovarian blood was greater when compounds were infused into a uterine lymphatic than into a uterine vein. Substantially more [3H]PGF2α occurred in the adjacent corpus luteum than either of the other compounds after a lymphatic infusion. Intra-lymphatic infusion of PGF2α stimulated the release of ovarian oxytocin but the effect was not confined to the adjacent ovary. Intravenous (jugular) infusion of PGF2α failed to stimulate ovarian oxytocin secretion whereas close-arterial infusion into the ovaries was effective, and the possibility was investigated that any systemic effect of PGF2α was mediated through neural mechanisms. Noradrenaline and acetylcholine were both effective in causing the release of ovarian oxytocin when infused close-arterially into the ovary. With infusions of acetylcholine, ovarian oxytocin secretion rate was increased over fivefold without any change in posterior pituitary release. Noradrenaline and acetylcholine produced a concomitant fall in ovarian blood flow, and neurotransmitter-induced ischaemia may have played a role in ovarian oxytocin release. The finding that PGF2α infused into a uterine lymphatic stimulates ovarian secretion of oxytocin, and that the effect is bilateral whereas PGF2α accumulation in ovarian tissue is unilateral, implies that its mechanism of action may not be solely directed at the luteal cell.
Journal of Endocrinology (1989) 122, 147–159
Opioid receptors on cells of the immune system: evidence for δ- and κ-classes
Authors: Carr D. J. J. , DeCosta B. R. , Kim C.-H. , Jacobson A. E. , Guarcello V. , Rice K. C. , Blalock J. E. 
Published: December 2008

ABSTRACT
Opioid peptides have been shown to modulate various parameters of both the humoral and cellular arms of the immune system. The modulatory capacity of the peptides can often be substantially reduced in the presence of naloxone, an opioid receptor antagonist, indicating a classical ligand-receptor interaction. In order to characterize these interactions further, we investigated the characteristics of opioid receptors on a macrophage cell line, P388d1. A δ-class opioid receptor was found with an Mr of 58 000. We also identified opioid receptors on MOLT-4 (T-cell) and IM-9 (B cell) cell lines as well as thymocytes and T celland B cell-enriched populations. Using the central (brain) κ-selective agonist, U-69,593, it was also determined that P388d1 cells possess κ-like opioid receptors. Scatchard analysis of the binding of [3H]U-69,593 revealed a single population of sites with a dissociation constant of 17 ± 3 (s.e.m.) nmol/l and a total number of binding sites of 53·8 ± 1·0 (s.e.m.) fmol/106 cells. Moreover, the racemic κ-selective agonist U-50,488H was able to displace 50% of [3H]U-69,593 binding at 8·0 nmol/l, whereas other opioid ligands such as [Met]-enkephalinamide (δ-selective) and [d-Ala2,N - Me - Phe4,Gly5 - ol] - enkephalin (μ - selective) were ineffective displacers of [3H]U-69,593 except at high concentrations.
Journal of Endocrinology (1989) 122, 161–168
Interleukin-1 inhibits thyrotrophin-induced human thyroglobulin gene expression
Authors: Yamashita S. , Kimura H. , Ashizawa K. , Nagayama Y. , Hirayu H. , Izumi M. , Nagataki S. 
Published: December 2008

ABSTRACT
The regulation of thyroglobulin (Tg) and its specific mRNA by interluekin-1 (IL-1) in cultured human thyrocytes was investigated. Specific binding of 125I-labelled IL-1 on thyrocytes was confirmed by solid-phase binding assay. Thyrocytes dispersed from Graves' thyroid tissues were incubated with TSH with or without recombinant human IL-1. TSH stimulated Tg release from cultured human thyrocytes in a dose- and time-dependent manner. Both IL-1α and β inhibited TSH-induced Tg release at concentrations ranging from 0·01 to 10 U/ml. The suppressive activities of IL-1α and β were similar. They did not alter the basal level of Tg release. Unstimulated human thyrocytes did not contain any detectable Tg mRNA, but TSH-stimulated thyrocytes expressed a single species of Tg mRNA (8·5 kb). Both IL-lα and β inhibited TSH-induced Tg mRNA in a dose-responsive manner. IL-1 (10 U/ml) caused maximal suppression of TSH-induced Tg mRNA to nearly basal levels. In contrast, the γ-actin mRNA hybridization signal was not altered in control or treated cells. Furthermore, IL-1 stimulated [3H]thymidine uptake into thyrocyte DNA. These results demonstrate that IL-1 directly inhibits TSH-induced Tg gene expression and provide further support for a functional role of IL-1 as a local modulator of thyroid hormone synthesis.
Journal of Endocrinology (1989) 122, 177–183
Metformin treatment of lean and obese Zucker rats modulates the ability of glucagon and insulin to regulate hepatocyte adenylate cyclase activity
Authors: Gawler D. J. , Wilson A. , Houslay M. D. 
Published: December 2008

ABSTRACT
Glucagon stimulated adenylate cyclase activity some 21-fold in liver membranes from lean (Fa/Fa) and some 20-fold in membranes from obese (fa/fa) Zucker rats, with constants yielding half-maximal activation (Ka values) of 12·6 and 120·1 nmol/l respectively. Treatment of animals with the biguanide drug metformin (N′,N′-dimethylbiguanide) decreased the ability of glucagon to stimulate this enzyme to some 16-fold for both the lean and obese animals and reduced the Ka values for activation of this enzyme by glucagon to 6·3 and 60·9 nmol/l respectively. Insulin inhibited glucagon-stimulated adenylate cyclase activity by some 24% in liver membranes from lean animals and some 17% in liver membranes from obese animals, with constants yielding half-maximal inhibition (Ki values) of 110 and 160 nmol/l respectively. The ability of insulin to inhibit the adenylate cyclase activity, from obese but not lean animals, was attenuated when insulin concentrations over 5 nmol/l were employed. Treatment of animals with metformin profoundly altered the sensitivity of adenylate cyclase to inhibition by insulin, with inhibition being increased to some 32% using liver membranes from either lean or obese animals. Values of Ki for this inhibitory action of insulin were 520 and 500 nmol/l using membranes from the lean and obese animals respectively, and no reduction in the ability of insulin, at concentrations over 5 nmol/l, to inhibit adenylate cyclase activity was observed using membranes from obese animals. Metformin also changed the kinetics of inhibition of adenylate cyclase by insulin. These were apparently negatively co-operative, with Hill coefficients of 0·76 and 0·89 using membranes from the untreated lean and obese animals respectively, and positively co-operative, with Hill coefficients of 1·45 and 1·20 for the metformin-treated lean and obese animals respectively.
Journal of Endocrinology (1989) 122, 207–212
Production of parathyroid hormone-like peptide in a human osteosarcoma cell line: stimulation by phorbol esters and epidermal growth factor
Authors: Rodan S. B. , Wesolowski G. , Ianacone J. , Thiede M. A. , Rodan G. A. 
Published: December 2008

ABSTRACT
A clonal cell line (Saos-2/B-10) derived from human osteosarcoma Saos-2 cells had the same osteoblastic characteristics as the mother line, but lacked sensitivity to parathyroid hormone (PTH) at early passages. At later passages (> 70) the cells became very sensitive to PTH (0·1 nmol/l). The absence of PTH-stimulatable adenylate cyclase correlated with the secretion of an adenylate cyclase-stimulatory activity which had the properties of the recently characterized PTH-like peptide (PTH-LP). This activity was inhibited by the PTH antagonist [8norleucyl, 18norleucyl, 34tyrosinyl]bovine PTH-(3–34)amide and could be neutralized by an antiserum raised against the synthetic PTH-LP-(1–34). Hybridization with a human PTH-LP cDNA showed that these cells produce two PTH-LP mRNAs of approximately 1·5 and 1·8 kb. The production of PTH-LP was stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA; 150 nmol/l) and epidermal growth factor (EGF; 10 ng/ml). The increased accumulation of PTH-LP in conditioned media in response to TPA was seen after 1 h and levelled off at 6 h. In contrast, EGF stimulation was lower at 3 and 6 h but continued for 24 h. Both agents increased PTH-LP mRNA levels in Saos-2/B-10 cells. A TPA analogue which does not stimulate protein kinase C had no effect on PTH-LP production. Cycloheximide blocked the stimulatory effect of both TPA and EGF and the TPA effect was blocked by actinomycin D, suggesting transcriptional control. The regulation of PTH-LP by these agents may offer clues regarding the association of this protein with malignancy.
Journal of Endocrinology (1989) 122, 219–227
Actions of parathyroid hormone-related protein on the rat kidney in vivo
Authors: Zhou H. , Leaver D. D. , Moseley J. M. , Kemp B. , Ebeling P. R. , Martin T. J. 
Published: December 2008

ABSTRACT
Peptides containing residues 1–34 of parathyroid hormone-related protein (PTHrP) and of bovine parathyroid hormone (bPTH), and recombinant full-length PTHrP(1–141) were infused i.v. into anaesthetized thyroparathyroidectomized rats to compare their action and potency on the renal handling of calcium, phosphate and cyclic AMP (cAMP) in vivo. All three peptides decreased the excretion of calcium and increased the excretion of phosphate and cAMP in the urine, with PTHrP(1–34) and PTHrP(1–141) having virtually equipotent effects. Thus the essential requirements for the major physiological activity of PTHrP on the kidney are contained within the 34 amino-terminal amino acids. For all three peptides, the lowest infusion rate that increased phosphate and cAMP excretion was 0·01 nmol/kg per h, whereas the lowest infusion rate that decreased calcium excretion was 0·025 nmol/kg per h for the PTHrP peptides and 0·1 nmol/kg per h for bPTH(1–34). The response to the PTHrP peptides was maximal at an infusion rate of 01 nmol/kg per h for both calcium and phosphate. Since the kidney is either equally sensitive to PTHrP and bPTH(1–34), or more sensitive to PTHrP than to bPTH(1–34), the hypercalcaemia of humoral hypercalcaemia of malignancy may develop because uncontrolled secretion of PTHrP increases the renal reabsorption of calcium to such an extent that even a modest increase in the inflow of calcium into the blood raises plasma calcium concentration.
Journal of Endocrinology (1989) 122, 229–235
Episodic secretion of inhibin into the ovarian vein during the follicular phase of the oestrous cycle in the ewe
Authors: McNeilly A. S. , Baird D. T. 
Published: December 2008

ABSTRACT
Changes in the plasma concentration of inhibin were measured by radioimmunoassay in ovarian venous blood collected at 10-min intervals for 5-h periods between 16 and 21 h and 40 and 45 h after cloprostenol-induced luteal regression in six Finn–Merino sheep. Episodes of inhibin secretion occurred with an interpulse interval of 66 ± 5 min in both stages of the follicular phase. These changes in inhibin were unrelated to pulses of LH or oestradiol. There was no relationship with plasma concentrations of FSH, which did not change in a pulsatile manner. These results suggest that the release of inhibin by the preovulatory follicle(s) occurs in a pulsatile manner and is under local control by unknown factors.
Journal of Endocrinology (1989) 122, 287–292
Inhibin and activin-like activity in fluids from male and female gonads: different molecular weight forms and bioactivity/immunoactivity ratios
Authors: Grootenhuis A. J. , Steenbergen J. , Timmerman M. A. , Dorsman A. N. R. D. , Schaaper W. M. M. , Meloen R. H. , de Jong F. H. 
Published: December 2008

ABSTRACT
The existence of various molecular weight forms of inhibin in ovarian follicular fluid has been reported earlier, while there is no information on the form of inhibin in testicular tissue. Inhibin bioactivity was therefore estimated in eluates of slices, obtained after SDS-PAGE of rat testicular and ovarian homogenates, rat Sertoli cell-conditioned medium (rSCCM) and bovine ovarian follicular fluid (bFF).
The only form of inhibin detected in testes from 22-day-old rats and in rSCCM was a 30 kDa protein. In rat ovarian extracts, larger forms of inhibin were also found as well as the predominant 30 kDa form. An activin-like activity was found in the 25 kDa SDS-PAGE eluates of both rSCCM and ovarian homogenates, which caused a dose-dependent increase of FSH release from cultured pituitary cells.
Activin-like activity and several forms of inhibin were found in bFF after SDS-PAGE. After purification of inhibin from bFF using dye affinity, anion-exchange, lentil lectin affinity chromatography and a subsequent reversed phase chromatography step, two pools of inhibin activity were obtained. These were separated by SDS-PAGE revealing 30 and 58 kDa inhibin forms. The immunoactivity of these forms of inhibin was then estimated using antibodies against the 22 N-terminal amino acids of the α subunit of 30 kDa bovine inhibin. It appeared that the two molecular weight forms of inhibin had bioactivity/immunoactivity ratios which differed more than five-fold. This indicates that results of radioimmunoassays of inhibin of ovarian origin, using peptide antisera, should be interpreted with caution.
Journal of Endocrinology (1989) 122, 293–301
Cellular basis of luteal steroidogenesis in the human ovary
Authors: Fisch B. , Margara R. A. , Winston R. M. L. , Hillier S. G. 
Published: December 2008

ABSTRACT
A primary monolayer cell culture system was developed to investigate human corpus luteum (CL) function in vitro. Steroidogenic cells were isolated by collagenase dispersal and Percoll density-gradient fractionation from CLs enucleated at progressive stages of the luteal phase (tubal surgery patients). 'Pure' granulosa-lutein cells were aspirated from ovulatory follicles at mid-cycle (in-vitro fertilization patients). The steroidogenic capacity (progesterone/20α-dihydroprogesterone biosynthesis and aromatase activity) of isolated luteal cells was assessed in relation to CL development. Basal luteal cell steroidogenesis was maximal at around the expected time of ovulation and declined with CL age during the luteal phase. Conversely, human chorionic gonadotrophin (hCG)-responsive steroidogenesis was initially undetectable but developed as the luteal phase progressed. These results show that luteal cell steroidogenesis becomes increasingly dependent upon gonadotrophic support with CL age. This is evidence that functional luteolysis in human ovaries (1) is pre-programmed to occur at the cellular level, (2) is initiated automatically at the time of ovulation and (3) is reversed at the time of CL 'rescue' in early pregnancy by the direct action of trophoblastic hCG on steroidogenic luteal cells. The culture system described should be of value in further defining the control of human CL form and function at the cellular level.
Journal of Endocrinology (1989) 122, 303–311
The inter-relationships between ovarian-independent growth, tumorigenicity, invasiveness and antioestrogen resistance in the malignant progression of human breast cancer
Authors: Clarke R. , Brünner N. , Thompson E. W. , Glanz P. , Katz D. , Dickson R. B. , Lippman M. E. 
Published: December 2008

ABSTRACT
Among the processes contributing to the progressive acquisition of the highly malignant phenotype in breast cancer are ovarian-independent growth, antioestrogen resistance and increased metastatic potential. We have previously observed that increased invasiveness and development of ovarian-independent growth occur independently. In an attempt to define the inter-relationships between these processes further, we have compared the phenotypes of ovarian-independent, invasive and antioestrogen-resistant sublines of the ovarian-dependent human breast cancer cell line MCF-7. Cells acquiring ovarian-independent growth can retain sensitivity to anti-oestrogens. One clone of MCF-7 cells selected for stable antioestrogen resistance has become non-tumorigenic but its invasive potential remains unaltered. Thus, acquisition of some characteristics of the progressed phenotype can occur independently. This phenomenon of independent parameters in phenotypic progression could partly explain the considerable intra- and intertumour heterogeneity characteristic of breast tumours.
Journal of Endocrinology (1989) 122, 331–340
Ultrastructural changes induced by oestradiol-17β, progesterone and oestrone-3-sulphate in guinea-pig endometrial glandular cells grown in primary culture
Authors: Alkhalaf M. , Chaminadas G. , Propper A. Y. , Adessi G. L. 
Published: December 2008

ABSTRACT
The effects of oestradiol-17β, progesterone and oestrone-3-sulphate were studied in primary cultures of guinea-pig endometrial glandular epithelial cells. Comparative ultrastructural studies were performed by means of transmission electron microscopy on cells grown either without hormones or with oestradiol-17β (2 nmol/l), oestradiol-17β (2 nmol/l) plus progesterone (50 nmol/l), or oestrone sulphate (0·1 μmol/l). In the control medium, without steroid hormones, the majority of epithelial cells were poorly differentiated, although numerous small mitochondria were present and abundant lipid droplets could be observed. Oestradiol-17β stimulated metabolic activity in the cells. Progesterone added to oestradiol-17β-primed cells stimulated the development of the endoplasmic reticulum–Golgi system. Oestrone sulphate induced a higher level of differentiation characterized by large clear mitochondria, well-developed Golgi complexes, and active nuclei, suggesting secretory activity. In all cases, the cultured cells displayed deep invaginations of the nuclear membrane associated with nuclear pores, known as nucleolar channels. After treatment with oestrone sulphate these channels were associated with a characteristic reticular nucleolus. We conclude that cultured endometrial epithelial cells display secretory activity in response to treatment with oestradiol-17β plus progesterone, or with oestrone sulphate.
Journal of Endocrinology (1989) 122, 439–444
Characterization of oxytocin receptors in rat adenohypophysis using a radioiodinated receptor antagonist peptide
Authors: Chadio S. E. , Antoni F. A. 
Published: December 2008

ABSTRACT
Oxytocin may function as a hypothalamic releasing hormone for prolactin and ACTH secretion in the rat. In the present study we have investigated the properties of putative oxytocin receptors in the rat adenohypophysis by radioligand-binding assay.
A novel oxytocin receptor antagonist [1-(β-mercapto-β,β-cyclopentamethylene propionic acid),2-(ortho-methyl)-Tyr2-Thr4-Orn8-Tyr9-NH2]-vasotocin (OTA) was radioiodinated by the iodogen method to a specific activity of 0·6 nCi/fmol. The radioiodinated derivative 125I-labelled OTA (125I-OTA) was reacted with membrane suspensions prepared from the uterus or adenohypophysis of female rats which were (a) ovariectomized for 7 days, (b) ovariectomized and treated with 5 μg oestradiol-17β 48 h before death or (c) implanted with a piece of silicone elastomer tubing containing 50 mg diethylstilboestrol (DES) 5 days before death. In uterine as well as the pituitary membrane suspensions, the radioligand was bound reversibly and with high affinity (dissociation constants 0·2 ± 0·1 and 0·1±0·01 nmol/l respectively; means + s.e.m., n=3) to a single class of sites with limited binding capacity, which varied with the type of pretreatment. Oestradiol-17β increased the binding capacity fivefold in the uterus in ovariectomized rats, but only very low specific radioligand binding was found in pituitary preparations from the same animals. Treatment with DES markedly increased the number of receptors in both the uterus and the adenohypophysis. Studies with several agonist and antagonist analogues revealed no difference in the ligand specificity of the uterine and adenohypophysial sites binding 125I-OTA, indicating that they are the same species of receptor. Furthermore, ligand-binding studies, carried out with tritiated vasopressin as tracer in pituitary membrane preparations, showed that OTA is not bound by pituitary vasopressin receptors at concentrations below 1 μmol/l.
In summary, 125I-OTA is a highly specific radioligand suitable for the analysis of pituitary oxytocin receptors. The low number of oxytocin receptors in the adenohypophysis of rats treated with oestradiol-17β suggests that the prolactin-stimulating action of oxytocin is mediated by highly efficient transmembrane signalling.
Journal of Endocrinology (1989) 122, 465–470
Burmese Russell's viper venom causes hormone release from rat pituitary cells in vitro
Authors: Hart G. R. , Proby C. , Dedhia G. , Yeo T. H. , Joplin G. F. , Burrin J. M. 
Published: December 2008

ABSTRACT
Acute and chronic hypopituitarism is associated with severe envenoming by the Burmese Russell's viper. We have demonstrated that in vitro, Burmese Russell's viper venom (0·1–10 μg/ml) causes a dose-dependent release of GH, TSH and ACTH from dispersed rat anterior pituitary cells in culture. At 10 μg/ml, venom causes a significant increase in the release of GH (344%, P<0·001), TSH (168%, P<0·005) and ACTH (>700%, P<0·001). We have also shown that the component (or components) responsible for this stimulatory effect is stable to heat (60 °C, 1 h) and mild trypsinization. Repeated addition of venom (1 μg/ml) to pituitary cells in a perifusion column system demonstrated attenuation of GH release. This reduced response was not due to depletion of the GH pool since the pituitary cells were subsequently able to respond to both GH-releasing factor (GRF) stimulation and KCl depolarization. Somatostatin in a dose which abolished GRF-stimulated GH release failed to affect venom-stimulated GH release, implying that venom acts in a cyclic AMP-independent manner. We conclude that Burmese Russell's viper venom has direct effects on pituitary hormone release in vitro. Whether these effects contribute to its known actions in vivo on the function of the pituitary remains to be established.
Journal of Endocrinology (1989) 122, 489–494