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  • 2000-2004  (4)
  • 1970-1974  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Evidence From Studies on Co-Cultures of TtT/GF and AtT20 Cells That Annexin 1 Acts as a Paracrine or Juxtacrine Mediator of the Early Inhibitory Effects of Glucocorticoids on ACTH Release (2003)
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Annexin 1 (ANXA1) is a key mediator of the inhibitory effects of glucocorticoids on adrenocorticotropic hormone (ACTH) release, which develop within 1–2 h of a steroid challenge. Our previous studies, which showed that (i) ANXA1 is expressed principally by the nonsecretory folliculo-stellate cells in the pituitary gland; (ii) glucocorticoids cause the exportation of ANXA1 from these cells; and (iii) corticotrophs express specific ANXA1 binding sites, led us to propose that ANXA1 serves as a paracrine or juxtacrine mediator of glucocorticoids. To address this hypothesis, we examined ANXA1-dependent glucocorticoid actions in co-cultures of murine corticotroph (AtT20 clone D1) and folliculo-stellate (TtT/GF) cell lines. ANXA1 mRNA and protein were found in abundance in TtT/GF cells but neither was detectable in the AtT20 cells. AtT20 cells (alone and in co-culture with TtT/GF cells) responded to corticotropin-releasing hormone (CRH) (0.1–1 µm) with increased ACTH release. The CRH-stimulated release of ACTH from AtT20 cells cultured alone was unaffected by preincubation with dexamethasone (Dex, 100 nm); by contrast, in co-cultures of AtT20 and TtT/GF cells, the steroid readily inhibited the secretory response to CRH. The effects of Dex on ACTH release were mimicked by N-terminal ANXA1 fragments (ANXA1Ac2−26, 2 µg/ml and ANXA11-188, 0.1 ng/ml) and reversed by mifepristone (1 µm) and by an antisense oligodeoxynucleotide (ODN) to ANXA1 (50 nm) but not by control ODNs. The antisense ODN also specifically blocked the Dex-induced externalization of ANXA1 from TtT/GF cells. Immunofluorescence imaging of the co-cultures localized the exported protein to the vicinity of the AtT20 cells and identified ANXA1 binding sites on these cells. These results provide functional and histological evidence to support our premise that the early inhibitory effects of glucocorticoids on ACTH release are dependent upon paracrine/juxtacrine actions of ANXA1 derived from folliculo-stellate cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.2003.01111.x
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  • 2
    Electronic Resource
    Electronic Resource
    Magnocellular Dendrites: Prototypic Receiver/Transmitters (2004)
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 16 (2004), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The hypothalamic magnocellular neurones of the supraoptic and paraventricular nuclei of mammals are among the best understood of all peptidergic neurones, and therefore serve as a model for understanding the functions of other peptidergic neurones. The release of vasopressin- and oxytocin-containing neurosecretory vesicles from their dendrites was first established 15 years ago. This local release is now known to have many functions, including controlling the interactions between oxytocin neurones and their surrounding glia, and facilitating and inhibiting the electrical activation of the neurones. Technical advances now permit dynamic analysis of dendritic release. Here, we review recent studies that focus on the conditional priming of dendritic peptide release by peptide-induced liberation of intracellular calcium, and the role of dendritic protein synthesis in the dendritic peptide release and the control of receptive properties of the neurones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0953-8194.2004.01182.x
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  • 3
    Electronic Resource
    Electronic Resource
    Annexin-1 (Lipocortin-1)-Immunoreactivity in the Folliculo-Stellate Cells of Rat Anterior Pituitary: The Effect of Adrenalectomy and Corticosterone Treatment on Its Subcellular Distribution (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neuroendocrinology 14 (2002), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In the pituitary gland, annexin-1 (lipocortin-1) located in folliculo-stellate (FS) cells has been advocated as one of the candidates for paracrine agents produced by FS cells that modulate the release of pituitary hormones. However, the expression and distribution pattern of annexin-1 in FS cells under different circulating corticosteroid conditions has not been examined. Thus, by means of pre-embedding immunoelectron microscopy, we investigated the expression of annexin-1 in FS cells under different corticosteroid conditions. Annexin-1-immunoreactivity was observed in the cytoplasm; especially intense immunoreactivity was detected in the follicle surface of FS cells under control conditions. After adrenalectomy, annexin-1-immunoreactivity almost disappeared, but the immunoreactivity recovered with corticosterone replacement. The expression of glucocorticoid receptor immunoreactivity in the nucleus of FS cells also showed a similar pattern to annexin-1 associated with the changes in the corticosteroid conditions. However, S-100 immunoreactivity, a marker for FS cells, was not changed whatever the corticosteroid conditions. These results confirm that glucocorticoids regulate the annexin-1 expression and demonstrate the translocation of annexin-1 from intracellular to pericellular sites in the FS cells of the rat anterior pituitary gland.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2002.00814.x
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  • 4
    Electronic Resource
    Electronic Resource
    Kinase-Dependent Regulation of the Secretion of Thyrotrophin and Luteinizing Hormone By Glucocorticoids and Annexin 1 Peptides (2003)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 15 (2003), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Our previous studies have identified a role for annexin 1 (ANXA1), a protein produced by the pituitary folliculostellate cells, as a paracrine/juxtacrine mediator of the acute regulatory effects of glucocorticoids on the release of adrenocorticotropic hormone and other pituitary hormones. In the present study, we focused on the secretion of thyroid stimulating hormone (TSH) and luteinizing hormone (LH) and used a battery of ANXA1-derived peptides to identify the key domains in the ANXA1 molecule that are critical to the inhibition of peptide release. In addition, as ANXA1 is a substrate for protein kinase C (PKC) and tyrosine kinase, we examined the roles of these kinases in the manifestation of the ANXA1-dependent inhibitory actions of dexamethasone on TSH and LH release. Dexamethasone suppressed the forskolin-induced release of TSH and LH from rat anterior pituitary tissue in vitro. Its effects were mimicked by human recombinant ANXA1 (hrANXA1) and a truncated protein, ANXA11-188. ANXA1Ac2−26, also suppressed stimulated peptide release but it lacked both the potency and the efficacy of the parent protein. Shorter N-terminal ANXA1 sequences were without effect. The PKC inhibitor PKC19-36 abolished the inhibitory actions of dexamethasone on the forskolin-evoked release of TSH and LH; it also attenuated the inhibitory actions of ANXA1Ac2−26. Similar effects were produced by annexin 5 (ANXA5) which sequesters PKC in other systems. By contrast, the tyrosine kinase inhibitors, p60v-src (137–157) and genistein, had no effect on the secretion of TSH or LH alone or in the presence of forskolin and/or dexamethasone. Dexamethasone caused the translocation of a tyrosine-phosphorylated species of ANXA1 to the surface of pituitary cells. The total amount of ANXA1 exported from the cells in response to the steroid was unaffected by tyrosine kinase blockade. However, the degree of tyrosine-phosphorylation of the exported protein was markedly reduced by genistein. These results suggest that (i) the ANXA1-dependent inhibitory actions of dexamethasone on the release of TSH and LH require PKC and sequences in the N-terminal domain of ANXA1, but are independent of tyrosine kinase, and (ii) while dexamethasone induces the cellular exportation of a tyrosine-phosphorylated species of ANXA1, tyrosine phosphorylation per se is not critical to the steroid-induced passage of ANXA1 across the membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2826.2003.01081.x
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  • 5
    Electronic Resource
    Electronic Resource
    A quantitative study of the ultrastructural changes in the hypothalamo-neurohypophysial system during and after experimentally induced hypersecretion (1974)
    Springer
    Cell & tissue research 149 (1974), S. 525-535 
    Details
    ISSN: 1432-0878
    Keywords: Supraoptic and paraventricular nuclei ; Ultrastructure ; Osmotic stimulus ; Quantitative study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Substitution of a 2% solution of sodium chloride in place of drinking water for 3 days significantly increased both the size of neurosecretory neurones in the supraoptic and paraventricular nuclei of rats and the proportion of these cells which had dilated endoplasmic reticulum. There was an increase in the number of multivesicular bodies per mean cell profile and also an increase in the ratio of “dense” (immature) to “pale” (mature) neurosecretory granules within the perikarya, although the total numbers of granules were unchanged. If, after 3 days of saline-treatment, the rats were again allowed tap water to drink for 2 days, the proportion of cells showing dilated endoplasmic reticulum and the number of multivesicular bodies returned towards normal, but there was a significant increase in the number of large dense lysosomal bodies per cell profile and a relative increase in the proportion of “pale” (mature) neurosecretory granules. These changes suggest that the increased bio-synthetic activity resulting from saline-treatment subsides when the treatment is terminated. Furthermore, since neurohypophysial hormone stores have still not returned to normal in animals of the recovery group, they also imply the absence of an internal feedback system by which the level of neural lobe hormone stores might govern the synthetic activity of the neurosecretory cells. Both the increased synthesis, and the increased electrical activity which accompanies it, may be independent consequences of the depleting stimulus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00223030
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