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  • 1
    Online Resource
    Online Resource
    Leukemia inhibitory factor regulates glucocorticoid receptor expression in the hypothalamic-pituitary-adrenal axis
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 289, No. 5 ( 2005-11), p. E857-E863
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 289, No. 5 ( 2005-11), p. E857-E863
    Abstract: Leukemia inhibitory factor (LIF) is a pleiotropic cytokine belonging to the gp130 family. LIF is induced peripherally and within the brain during inflammatory or chronic autoimmune diseases and is a potent stimulator of the hypothalamic-pituitary-adrenal (HPA) axis. Here we investigated the role of LIF in mediating glucocorticoid receptor (GR) expression in the HPA axis. LIF treatment (3 μg/mouse, ip) markedly decreased GR mRNA levels in murine hypothalamus (5-fold, P 〈 0.01) and pituitary (1.7-fold, P 〈 0.01) and downregulated GR protein levels. LIF decreased GR expression in murine corticotroph cell line AtT20 within 2 h, and this effect was sustained for 8 h after treatment. LIF-induced GR mRNA reduction was abrogated in AtT20 cells overexpressing dominant-negative mutants of STAT3, indicating that intact JAK-STAT signaling is required to mediate LIF effects on GR expression. Conversely, mice with LIF deficiency exhibited increased GR mRNA levels in the hypothalamus and pituitary (3.5- and 3.5-fold, respectively; P 〈 0.01 for both) and increased GR protein expression when compared with wild-type littermates. The suppressive effects of dexamethasone on GR were more pronounced in LIF-null animals. These data suggest that LIF maintains the HPA axis activation by decreasing GR expression and raise the possibility that LIF might contribute to the development of central glucocorticoid resistance during inflammation.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00577.2004
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Senescence Mediates Pituitary Hypoplasia and Restrains Pituitary Tumor Growth
    American Association for Cancer Research (AACR) ; 2007
    In:  Cancer Research Vol. 67, No. 21 ( 2007-11-01), p. 10564-10572
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 67, No. 21 ( 2007-11-01), p. 10564-10572
    Abstract: Understanding factors subserving pituitary cell proliferation enables understanding mechanisms underlying uniquely benign pituitary tumors. Pituitary tumor-transforming gene (Pttg) deletion results in pituitary hypoplasia, low pituitary cell proliferation rates, and rescue of pituitary tumor development in Rb+/− mice. Pttg−/− pituitary glands exhibit ARF/p53/p21-dependent senescence pathway activation evidenced by up-regulated p19, cyclin D1, and Bcl-2 protein levels and p53 stabilization. High pituitary p21 levels in the absence of PTTG were associated with suppressed cyclin-dependent kinase 2 activity, Rb phosphorylation, and cyclin A expression, all required for cell cycle progression. Although senescence-associated β-galactosidase was enhanced in Pttg-deficient pituitary glands, telomere lengths were increased. DNA damage signaling pathways were activated and aneuploidy was evident in the Pttg-deficient pituitary, triggering senescence-associated genes. To confirm the p21 dependency of decreased proliferation and senescence in the Pttg-null pituitary, mouse embryonic fibroblast (MEF) colony formation was tested in wild-type, Pttg−/−, Rb+/−, Rb+/−Pttg−/−, and Rb+/−Pttg−/−p21−/− cells. Rb+/−Pttg−/− MEFs, unlike Rb+/− cells, failed to produce colonies and exhibited high levels of senescence. p21 deletion from Rb+/−Pttg−/− MEFs enhanced anchorage-independent cell growth, accompanied by a marked decrease in senescence. As cell proliferation assessed by bromodeoxyuridine incorporation was higher in Rb+/−Pttg−/−p21−/− relative to Rb+/−Pttg−/− pituitary glands, p21-dependent senescence provoked by Pttg deletion may underlie pituitary hypoplasia and decreased tumor development in Rb+/−Pttg−/− mice. [Cancer Res 2007;67(21):10564–72]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-07-0974
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2007
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
    Online Resource
    Online Resource
    Leukemia inhibitory factor signaling is implicated in embrionic development of the HPA axis
    Wiley ; 2005
    In:  FEBS Letters Vol. 579, No. 20 ( 2005-08-15), p. 4465-4469
    Details
    In: FEBS Letters, Wiley, Vol. 579, No. 20 ( 2005-08-15), p. 4465-4469
    Type of Medium: Online Resource
    ISSN: 0014-5793
    URL: Article
    DOI: 10.1016/j.febslet.2005.07.014
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    p21 Cip1 restricts neuronal proliferation in the subgranular zone of the dentate gyrus of the hippocampus
    Proceedings of the National Academy of Sciences ; 2008
    In:  Proceedings of the National Academy of Sciences Vol. 105, No. 4 ( 2008-01-29), p. 1358-1363
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 105, No. 4 ( 2008-01-29), p. 1358-1363
    Abstract: The subgranular zone (SGZ) of the dentate gyrus of the hippocampus is a brain region where robust neurogenesis continues throughout adulthood. Cyclin-dependent kinases (CDKs) have a primary role in controlling cell division and cellular proliferation. p21 Cip1 (p21) is a CDK inhibitor that restrains cell cycle progression. Confocal microscopy revealed that p21 is abundantly expressed in the nuclei of cells in the SGZ and is colocalized with NeuN, a marker for neurons. Doublecortin (DCX) is a cytoskeletal protein that is primarily expressed by neuroblasts. By using FACS analysis it was found that, among DCX-positive cells, 42.8% stained for p21, indicating that p21 is expressed in neuroblasts and in newly developing neurons. p21-null ( p21 −/− ) mice were examined, and the rate of cellular proliferation, as measured by BrdU incorporation, was increased in the SGZ of p21 −/− compared with WT mice. In addition, the levels of both DCX and NeuN protein were increased in p21 −/− mice, further demonstrating increased hippocampal neuron proliferation. Chronic treatment with the tricyclic antidepressant imipramine (10 mg/kg per day i.p. for 21 days) markedly decreased hippocampal p21 mRNA and protein levels, produced antidepressant-like behavioral changes in the forced swim test, and stimulated neurogenesis in the hippocampus. These results suggest that p21 restrains neurogenesis in the SGZ and imipramine-induced stimulation of neurogenesis might be a consequence of decreased p21 expression and the subsequent release of neuronal progenitor cells from the blockade of proliferation. Because many antidepressants stimulate neurogenesis, it is possible that their shared common mechanism of action is suppression of p21.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0711030105
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2008
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Diminished Pancreatic β-Cell Mass in Securin-Null Mice Is Caused by β-Cell Apoptosis and Senescence
    The Endocrine Society ; 2009
    In:  Endocrinology Vol. 150, No. 6 ( 2009-06-01), p. 2603-2610
    Details
    In: Endocrinology, The Endocrine Society, Vol. 150, No. 6 ( 2009-06-01), p. 2603-2610
    Type of Medium: Online Resource
    ISSN: 0013-7227 , 1945-7170
    URL: Article
    DOI: 10.1210/en.2008-0972
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2009
    detail.hit.zdb_id: 2011695-0
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  • 6
    Online Resource
    Online Resource
    p21 Cip1 restrains pituitary tumor growth
    Proceedings of the National Academy of Sciences ; 2008
    In:  Proceedings of the National Academy of Sciences Vol. 105, No. 45 ( 2008-11-11), p. 17498-17503
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 105, No. 45 ( 2008-11-11), p. 17498-17503
    Abstract: As commonly encountered, pituitary adenomas are invariably benign. We therefore studied protective pituitary proliferative mechanisms. Pituitary tumor transforming gene ( Pttg ) deletion results in pituitary p21 induction and abrogates tumor development in Rb +/− Pttg −/− mice. p21 disruption restores attenuated Rb +/− Pttg −/− pituitary proliferation rates and enables high penetrance of pituitary, but not thyroid, tumor growth in triple mutant animals (88% of Rb +/− and 72% of Rb +/− Pttg −/− p21 −/− vs. 30% of Rb +/− Pttg −/− mice developed pituitary tumors, P 〈 0.001). p21 deletion also accelerated S-phase entry and enhanced transformation rates in triple mutant MEFs. Intranuclear p21 accumulates in Pttg -null aneuploid GH-secreting cells, and GH 3 rat pituitary tumor cells overexpressing PTTG also exhibited increased levels of mRNA for both p21 (18-fold, P 〈 0.01) and ATM (9-fold, P 〈 0.01). PTTG is abundantly expressed in human pituitary tumors, and in 23 of 26 GH-producing pituitary adenomas with high PTTG levels, senescence was evidenced by increased p21 and SA-β-galactosidase. Thus, either deletion or overexpression of Pttg promotes pituitary cell aneuploidy and p53/p21-dependent senescence, particularly in GH-secreting cells. Aneuploid pituitary cell p21 may constrain pituitary tumor growth, thus accounting for the very low incidence of pituitary carcinomas.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0804810105
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2008
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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  • 7
    Online Resource
    Online Resource
    Pituitary Hypoplasia in Pttg −/− Mice Is Protective for Rb +/− Pituitary Tumorigenesis
    The Endocrine Society ; 2005
    In:  Molecular Endocrinology Vol. 19, No. 9 ( 2005-09), p. 2371-2379
    Details
    In: Molecular Endocrinology, The Endocrine Society, Vol. 19, No. 9 ( 2005-09), p. 2371-2379
    Type of Medium: Online Resource
    ISSN: 0888-8809 , 1944-9917
    URL: Article
    DOI: 10.1210/me.2005-0137
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2005
    detail.hit.zdb_id: 1492112-1
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