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  • Bioscientifica  (24)
  • 1995-1999  (24)
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  • Bioscientifica  (24)
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  • 1995-1999  (24)
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  • 1
    Online Resource
    Online Resource
    Fetal expression of GnRH and GnRH receptor genes in rat testis and ovary
    Bioscientifica ; 1998
    In:  Journal of Endocrinology Vol. 159, No. 1 ( 1998-10-1), p. 179-189
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 159, No. 1 ( 1998-10-1), p. 179-189
    Abstract: The identification of gonadal gonadotropin-releasing hormone receptors (GnRH-R) and evidence of direct inhibitory effects of GnRH agonists upon steroidogenesis in adult rat gonads, lend credence to a putative intragonadal role of a locally secreted GnRH or GnRH-like peptide. Using reverse transcription-polymerase chain reaction followed by Southern blot hybridization and sequencing, we identified, both in the ovary and in the testis of fetal and adult rats, a fully processed GnRH messenger RNA (mRNA), the sequence of which, in adult testis, was identical to that found in the hypothalamus. We also detected in the testis, but not in the ovary, a transcript containing the first intron. The ontogeny of GnRH and GnRH-R gene expression was studied in rat gonads from 14.5 to 21.5 days post-coitum (dpc), using dot blot hybridization of total RNA. During this period, the levels of cyclophilin mRNA normalized to total RNA remained unchanged. Thus, we used cyclophilin as an internal standard. GnRH mRNA was detected in the ovary at 18.5 dpc, four days later than in the testis, and similar levels were found in both sexes at birth. GnRH-R mRNA was present at 14.5 dpc in the testis and at 15.5 dpc in the ovary, with the levels at 21.5 dpc being 2.4 times higher in the testis than in the ovary. GnRH and GnRH-R mRNA levels increased in both sexes in late fetal development, but this increase appeared two days sooner in the ovary compared with the testis, thus supporting the hypothesis that expression of the GnRH and GnRH-R genes is regulated in a sex-dependent manner during fetal development. In all cases, expression of GnRH and GnRH-R preceded gonadotropin receptors in the gonads and initiation of gonadotropin secretion by the pituitary.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1590179
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1998
    detail.hit.zdb_id: 1474892-7
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  • 2
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    Online Resource
    Ovine chorionic somatomammotrophin (oCS) production by isolated cotyledon cells from sheep in early and mid gestation: auto-regulation by recombinant oCS
    Bioscientifica ; 1999
    In:  Journal of Endocrinology Vol. 161, No. 2 ( 1999-05-1), p. 289-298
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 161, No. 2 ( 1999-05-1), p. 289-298
    Abstract: We report the ability of sheep placental cotyledonary cells, isolated at different periods of pregnancy (40 to 90 days) to produce ovine chorionic somatomammotrophin (oCS) in in vitro culture conditions. This oCS production increased gradually with stage of pregnancy. Endogenous oCS net production by isolated placental cells was increased, in a dose-dependent manner, by addition of recombinant oCS (roCS). This effect was not observed after addition of recombinant ovine growth hormone. The roCS effect was more potent on cells collected during early pregnancy. Specific immunoprecipitation of oCS revealed that roCS treatment was associated with an increased dose-dependent incorporation of [35S] methionine-[35S]cysteine. These findings provide evidence that oCS may act in a paracrine/autocrine manner to up-regulate its own production during early gestation. We suggest that this autoregulation may be associated with morphological and functional differentiation of the trophoblast during the growth of the placenta.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1610289
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1999
    detail.hit.zdb_id: 1474892-7
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  • 3
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    Online Resource
    Characterization of 11beta-hydroxysteroid dehydrogenase activity and corticosteroid receptor expression in human osteosarcoma cell lines
    Bioscientifica ; 1999
    In:  Journal of Endocrinology Vol. 161, No. 3 ( 1999-06-1), p. 455-464
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 161, No. 3 ( 1999-06-1), p. 455-464
    Abstract: Studies in vitro and in vivo have shown that corticosteroids play an important role in bone physiology and pathophysiology. It is now established that corticosteroid hormone action is regulated, in part, at the pre-receptor level through the expression of isozymes of 11beta-hydroxysteroid dehydrogenase (11beta-HSD), which are responsible for the interconversion of hormonally active cortisol to cortisone. In this report we demonstrate 11beta-HSD activity in human osteoblast (OB) cells. Osteosarcoma-derived OB cell lines TE-85, MG-63 and SaOS-2 and fibrosarcoma Hs913T cells express the type 2 isoform of 11beta-HSD, as determined by reverse transcription polymerase chain reaction (RT-PCR) and specific enzyme assays. Enzyme activity was shown to be strictly NAD dependent with a Km of approximately 71 nM; 11beta-HSD type 1 mRNA expression and enzyme activity were not detected. All four cell lines expressed mRNA for the glucocorticoid receptor (GR) and mineralocorticoid receptor, but specific binding was only detectable with radiolabelled dexamethasone (Kd=10 nM) and not aldosterone. MG-63 cells had two to three times more GR than the other OB cells, which correlated with the higher levels of 11beta-HSD 2 activity in these cells. In contrast to the osteosarcoma cell studies, RT-PCR analysis of primary cultures of human OB cells revealed the presence of mRNA for 11beta-HSD 1 as well as 11beta-HSD 2. However, enzyme activity in these cells remained predominantly oxidative, i.e. inactivation of cortisol to cortisone (147 pmol/h per mg protein at 500 nM cortisol) was greater than cortisone to cortisol (10.3 pmol/h per mg protein at 250 nM cortisone). Data from normal human OB and osteosarcoma cells demonstrate the presence of an endogenous mechanism for inactivation of glucocorticoids in OB cells. We postulate that expression of the type 1 and type 2 isoforms of 11beta-HSD in human bone plays an important role in normal bone homeostasis, and may be implicated in the pathogenesis of steroid-induced osteoporosis.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1610455
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1999
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  • 4
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    Online Resource
    Growth factors and goitrogenesis
    Bioscientifica ; 1999
    In:  Journal of Endocrinology Vol. 160, No. 3 ( 1999-03-1), p. 321-332
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 160, No. 3 ( 1999-03-1), p. 321-332
    Abstract: By combining data from studies of multinodular non-toxic goitre (MNTG) with data from rat models of goitre induction and in vitro models, a map of the growth factors involved in goitrogenesis has been constructed. We have addressed the roles of the insulin-like growth factors, transforming growth factors, fibroblast growth factors, endothelins, etc. We hypothesise that an imbalance in the interactions between the various growth factor axes exists in MNTG which favours cell replication. Thyrotrophin, although not significantly elevated in MNTG, exerts critical effects through interactions with autocrine and paracrine factors and their receptors. Expansion of the thyroidal vascular bed through angiogenesis is closely co-ordinated with follicular cell expansion and folliculoneogenesis, and while the integrated paracrine actions of fibroblast growth factors, vascular endothelial growth factor and endothelin probably play central roles, additional, as yet elusive, factors are probably involved. The combination of in vitro and in vivo approaches, designed to address specific questions, will undoubtedly continue to prove invaluable in dissecting further the complex interactions that exist between these growth factors, their binding proteins and receptors in goitrogenesis.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1600321
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1999
    detail.hit.zdb_id: 1474892-7
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  • 5
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    Online Resource
    LH down-regulates gonadotropin-releasing hormone (GnRH) receptor, but not GnRH, mRNA levels in the rat testis
    Bioscientifica ; 1999
    In:  Journal of Endocrinology Vol. 162, No. 3 ( 1999-09-1), p. 409-415
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 162, No. 3 ( 1999-09-1), p. 409-415
    Abstract: The demonstration of an inhibitory effect of gonadotropin-releasing hormone (GnRH) agonists upon steroidogenesis in hypophysectomized rats and the presence of mRNA coding for GnRH and GnRH receptors (GnRH-R) in rat gonads suggests that GnRH can act locally in the gonads. To assess this hypothesis, we investigated the effects of GnRH analogs, gonadotropins and testosterone on the levels of both GnRH and GnRH-R mRNA in the rat testis. Using dot blot hybridization, we measured the mRNA levels 2 to 120 h after the administration of the GnRH agonist, triptorelin. We observed an acute reduction of both GnRH and GnRH-R mRNAs 24 h after the injection (about 38% of control). However, the kinetics for testis GnRH-R mRNA were different from those previously found for pituitary GnRH-R mRNA under the same conditions. Initially, the concentrations of serum LH and FSH peaked, then declined, probably due to the desensitization of the gonadotrope cells. In contrast, the GnRH antagonist, antarelix, after 8 h induced a 2.5-fold increase in GnRH-R mRNA, but not in GnRH mRNA, while gonadotropins levels were reduced. Human recombinant FSH had no significant effect on either GnRH or GnRH-R mRNA levels. Inversely, GnRH-R mRNA levels markedly decreased by 21% of that of control 24 h after hCG injection. Finally, 24 h after testosterone injection, a significant increase in GnRH-R mRNA levels (2.3 fold vs control) was found, but a reduction in the concentration of serum LH, probably by negative feedback on the pituitary, was observed. In contrast, GnRH mRNA levels were not significantly altered following testosterone treatment. Since LH receptors, GnRH-R and testosterone synthesis are colocalized in Leydig cells, our data suggest that LH could inhibit the GnRH-R gene expression or decrease the GnRH-R mRNA stability in the testis. However, this does not exclude the possibility that GnRH analogs could also affect the GnRH-R mRNA levels via direct binding to testicular GnRH-R. In contrast, the regulation of GnRH mRNA levels appeared to be independent of gonadotropins. Taken together, our results suggest a regulation of GnRH and GnRH-R mRNA specific for the testis.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1620409
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1999
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  • 6
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    Online Resource
    Hormone-induced changes in nuclear receptor stoichiometry in HL60 cells correlate with induction of monocyte or neutrophil differentiation
    Bioscientifica ; 1998
    In:  Journal of Endocrinology Vol. 156, No. 1 ( 1998-01-1), p. 135-148
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 156, No. 1 ( 1998-01-1), p. 135-148
    Abstract: HL60 cells differentiate to monocytes or neutrophils in response to 1 alpha,25(OH)2-vitamin D3 (D3) and retinoids respectively. D3 and retinoid actions converge since their receptors (VDR, RAR) heterodimerise with a common partner, RXR, which also interacts with thyroid hormone (T3) receptors (T3R). HL60 cells were treated with combinations of D3 and retinoids to induce differentiation and to investigate whether increased VDR or RAR expression correlated with monocyte or neutrophil differentiation and whether altered receptor concentrations affected DNA-binding specificity. As assessed by Western blotting, VDR and RXR expression was unchanged in monocytes relative to controls but levels of RAR and T3R were reduced. In contrast, only VDR expression was reduced in neutrophils. T3 did not promote differentiation or influence its induction by D3 or retinoids and did not affect expression of any receptor. Gel mobility-shift analysis revealed that nuclear extracts from undifferentiated cells, monocytes and neutrophils interacted differently with VDRE-, RARE- and RXRE-binding sites. Monocyte nuclear protein/DNA complexes contain readily detectable VDR and RXR whereas neutrophil complexes contain RAR and RXR. Thus hormone-induced changes in receptor stoichiometry favour either VDR/RXR or RAR/RXR heterodimerisation and correlate with hormone-induced differentiation of HL60 cells to monocytes or neutrophils respectively.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1560135
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1998
    detail.hit.zdb_id: 1474892-7
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  • 7
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    Online Resource
    Evidence for androgen receptor gene expression and growth inhibitory effect of dihydrotestosterone on human adrenocortical cells
    Bioscientifica ; 1998
    In:  Journal of Endocrinology Vol. 159, No. 3 ( 1998-12-1), p. 373-380
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 159, No. 3 ( 1998-12-1), p. 373-380
    Abstract: Evidence for the expression of the canonic androgen receptor (AR) in human adrenal cortex has not been provided so far. The aim of the present study was to demonstrate the expression of the AR gene in normal and neoplastic adrenocortical human tissues and in the human adrenocortical cancer cell line, NCI-H295, and then to evaluate the effect of dihydrotestosterone (DHT) on human adrenocortical cell growth. An AR cDNA fragment with the expected size of 262 bp was detected by using reverse transcription (RT)-PCR in normal and neoplastic adrenocortical human tissues and in the neoplastic cell line, demonstrating that the gene for AR is indeed expressed in human adrenal cells. In the human adrenocortical cancer cell line NCI-H295, DHT at physiological concentrations produced a significant reduction in cell proliferation and inhibition of colony formation in soft agar. The inhibitory effect on adrenocortical cell growth was evident after both 24 and 48 h of treatment. The antiandrogens, cyproterone acetate and hydroxyflutamide, were capable of reversing the effects exerted by DHT. The androgen-induced growth inhibitory effect was also detected in primary culture of three non-functioning adrenocortical adenomas. These findings show that the canonic AR is present in human adrenocortical cells and that androgens may have a role in the adrenal cortex by reducing cell proliferation.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1590373
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1998
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  • 8
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    Online Resource
    Specific receptors for synthetic GH secretagogues in the human brain and pituitary gland
    Bioscientifica ; 1998
    In:  Journal of Endocrinology Vol. 157, No. 1 ( 1998-04-1), p. 99-106
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 157, No. 1 ( 1998-04-1), p. 99-106
    Abstract: In vitro studies have been performed to demonstrate and characterize specific binding sites for synthetic GH secretagogues (sGHS) on membranes from pituitary gland and different human brain regions. A binding assay for sGHS was established using a peptidyl sGHS (Tyr-Ala-hexarelin) which had been radioiodinated to high specific activity at the Tyr residue. Specific binding sites for 125I-labelled Tyr-Ala-hexarelin were detected mainly in membranes isolated from pituitary gland and hypothalamus, but they were also present in other brain areas such as choroid plexus, cerebral cortex, hippocampus and medulla oblongata with no sex-related differences. In contrast, negligible binding was found in the thalamus, striatum, substantia nigra, cerebellum and corpus callosum. The binding of 125I-labelled Tyr-Ala-hexarelin to membrane-binding sites is a saturable and reversible process, depending on incubation time and pH of the buffer. Scatchard analysis of the binding revealed a finite number of binding sites in the hypothalamus and pituitary gland with a dissociation constant (Kd) of (1.5 +/- 0.3) x 10(-9) and (2.1 +/- 0.4) x 10(-9) mol/l respectively. Receptor activity is sensitive to trypsin and phospholipase C digestion, suggesting that protein and phospholipids are essential for the binding of 125I-labelled Tyr-Ala-hexarelin. The binding of 125I-labelled Tyr-Ala-hexarelin to pituitary and hypothalamic membranes was displaced in a dose-dependent manner by different unlabelled synthetic peptidyl (Tyr-Ala-hexarelin, GHRP2, hexarelin, GHRP6) and non-peptidyl (MK 0677) sGHS. An inhibition of the specific binding was also observed when binding was performed in the presence of [D-Arg1-D-Phe5-D-Trp7,9-Leu11]-substance P, a substance P antagonist that has been found to inhibit GH release in response to sGHS. In contrast, no competition was observed in the presence of other neuropeptides (GHRH, somatostatin, galanin or Met-enkephalin) which have a known influence on GH release. In conclusion, the present data demonstrate that sGHS have specific receptors in human brain and pituitary gland and reinforce the hypothesis that these compounds could be the synthetic counterpart of an endogenous GH secretagogue involved in the neuroendocrine control of GH secretion and possibly in other central activities.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1570099
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1998
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  • 9
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    Online Resource
    Effects of prolonged infusion of basic fibroblast growth factor and IGF-I on adrenocortical differentiation in the autotransplanted adrenal: an immunohistochemical study
    Bioscientifica ; 1999
    In:  Journal of Endocrinology Vol. 162, No. 1 ( 1999-07-1), p. 21-29
    Details
    In: Journal of Endocrinology, Bioscientifica, Vol. 162, No. 1 ( 1999-07-1), p. 21-29
    Abstract: Adrenocortical regeneration after adrenal autotransplantation provides a model for the study of local autocrine/paracrine mechanisms involved in the growth and differentiation of the adrenal cortex. To study the possible involvement of some growth factors, namely basic fibroblast growth factor (bFGF, FGF-2) and insulin-like growth factor I (IGF-I), in cell differentiation, immunohistochemical and ultrastructural studies were carried out on adrenal autotransplants in adult male rats. To distinguish between fasciculata and glomerulosa-like cells with accuracy, tissue sections were immunostained with IZAb, which recognizes the inner zone antigen (IZAg) present in fasciculata and reticularis cells but absent from the glomerulosa, and by electron microscopy. IGF-I-treated animals exhibited a clear glomerulosa-like zone that was devoid of IZAb immunostaining. In this outer subcapsular area, ultrastructural examination showed cells containing mitochondria with irregular cristae resembling those of the fetal or immature glomerulosa cells. In contrast, no significant morphological differences were observed in bFGF-treated animals when compared with those from saline-treated controls, in both of which, IZAb immunostaining occurred in almost all adrenocortical cells, with no clear zonation or glomerulosa, as seen in the intact animal. Plasma aldosterone and corticosterone concentrations were lower in autotransplanted control animals than in intact controls, although plasma renin activities were similar. IGF-I treatment significantly increased aldosterone concentrations, whereas corticosterone and plasma renin activity were reduced. bFGF infusion further reduced plasma aldosterone, although plasma renin activity and corticosterone were unaffected. These results suggest that the two growth factors have different effects on zonal differentiation and function in the autotransplanted gland. In particular, bFGF, by reducing glomerulosa function, appears partly to replicate the actions of ACTH in normal animals. In contrast, IGF-I enhances the glomerulosa secreting phenotype and diminishes that of the fasciculata/reticularis, possibly replicating the actions of angiotensin II or a low sodium diet.
    Type of Medium: Online Resource
    ISSN: 0022-0795 , 1479-6805
    URL: Article
    DOI: 10.1677/joe.0.1620021
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1999
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  • 10
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    Online Resource
    Repression of the acetyl-CoA carboxylase gene in ovine adipose tissue during lactation: the role of insulin responsiveness
    Bioscientifica ; 1997
    In:  Journal of Molecular Endocrinology Vol. 19, No. 2 ( 1997-10-1), p. 99-107
    Details
    In: Journal of Molecular Endocrinology, Bioscientifica, Vol. 19, No. 2 ( 1997-10-1), p. 99-107
    Abstract: We have investigated the mechanisms whereby lipogenesis is markedly suppressed in adipose tissue depots of lactating sheep. Expression of the gene encoding acetyl-CoA carboxylase (ACC), the flux-determining enzyme of the lipogenic pathway, is reduced approximately threefold in both omental and subcutaneous adipose tissue depots during late pregnancy and remains so into lactation when compared with non-pregnant, non-lactating animals. By comparison, total ACC enzyme activity in these adipose depots is suppressed approximately 25- to 30-fold in lactation. Culture of explants from the subcutaneous depot of lactating sheep with insulin plus dexamethasone for 72 h resulted in an approximately sevenfold increase in ACC mRNA, a fivefold increase in total enzyme activity and a marked increase in the proportion of the enzyme in the active state when compared with explants cultured with no added hormones for the same period. However, there was a lag of between 32 and 48 h before marked induction of any of these parameters by insulin plus dexamethasone was observed. Induction of the alpha-tubulin gene paralleled that of the ACC gene, suggesting that cytoskeletal rearrangements are associated with the aquisition of sensitivity to insulin plus dexamethasone. These results demonstrate that the reduction in lipogenic capacity in ovine adipose tissue during lactation is related to repression of the ACC gene, both at the level of steady-state mRNA abundance and possibly at translation, as well as to suppression of the mechanisms that regulate the proportion of ACC in the active state, and these are further related to the marked insensitivity of these parameters to insulin plus dexamethasone in vitro.
    Type of Medium: Online Resource
    ISSN: 0952-5041 , 1479-6813
    URL: Article
    DOI: 10.1677/jme.0.0190099
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 1997
    detail.hit.zdb_id: 1478171-2
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