The Experts below are selected from a list of 174 Experts worldwide ranked by ideXlab platform
Adriana Seilicovich - One of the best experts on this subject based on the ideXlab platform.
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Estradiol Upregulates c-FLIPlong Expression in Anterior Pituitary Cells.
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2015Co-Authors: Gabriela Jaita, Sandra Zárate, Jimena Ferraris, María Florencia Gottardo, Guadalupe Eijo, María Laura Magri, Daniel Pisera, Adriana SeilicovichAbstract:Anterior Pituitary cell turnover depends on a tight balance between proliferation and apoptosis. We have previously shown that estrogens sensitize Anterior Pituitary cells to pro-apoptotic stimuli. c-FLIP (cellular-FLICE-inhibitory-protein) isoforms are regulatory proteins of apoptosis triggered by death receptors. c-FLIPshort isoform competes with procaspase-8 inhibiting its activation. However, c-FLIPlong isoform may have a pro- or anti-apoptotic function depending on its expression level. In the present study, we explored whether estrogens modulate c-FLIP expression in Anterior Pituitary cells from ovariectomized (OVX) rats and in GH3 cells, a somatolactotrope cell line. Acute administration of 17β-estradiol to OVX rats increased c-FLIPlong expression in the Anterior Pituitary gland without changing c-FLIPshort expression as assessed by Western blot. Estradiol in vitro also increased c-FLIPlong expression in Anterior Pituitary cells but not in GH3 cells. As determined by flow cytometry, the percentage of Anterior Pituitary cells expressing c-FLIP was higher than in GH3 cells. However, c-FLIP fluorescence intensity in GH3 cells was higher than in Anterior Pituitary cells. FasL increased the percentage of TUNEL-positive GH3 cells incubated either with or without estradiol suggesting that the pro-apoptotic action of Fas activation is estrogen-independent. Our results show that unlike what happens in nontumoral Pituitary cells, estrogens do not modulate either c-FLIPlong expression or FasL-induced apoptosis in GH3 cells. The stimulatory effect of estradiol on c-FLIPlong expression could be involved in the sensitizing effect of this steroid to apoptosis in Anterior Pituitary cells. The absence of this estrogenic action in tumor Pituitary cells could be involved in their tumor-like behavior.
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N-terminal prolactin-derived fragments, vasoinhibins, are proapoptoptic and antiproliferative in the Anterior Pituitary.
PloS one, 2011Co-Authors: Jimena Ferraris, Verónica Zaldivar, Gabriela Jaita, Adriana Seilicovich, Sandra Zárate, Guadalupe Eijo, Daniela Radl, Carmen Clapp, Daniel PiseraAbstract:The Anterior Pituitary is under a constant cell turnover modulated by gonadal steroids. In the rat, an increase in the rate of apoptosis occurs at proestrus whereas a peak of proliferation takes place at estrus. At proestrus, concomitant with the maximum rate of apoptosis, a peak in circulating levels of prolactin is observed. Prolactin can be cleaved to different N-terminal fragments, vasoinhibins, which are proapoptotic and antiproliferative factors for endothelial cells. It was reported that a 16 kDa vasoinhibin is produced in the rat Anterior Pituitary by cathepsin D. In the present study we investigated the Anterior Pituitary production of N-terminal prolactin-derived fragments along the estrous cycle and the involvement of estrogens in this process. In addition, we studied the effects of a recombinant vasoinhibin, 16 kDa prolactin, on Anterior Pituitary apoptosis and proliferation. We observed by Western Blot that N-terminal prolactin-derived fragments production in the Anterior Pituitary was higher at proestrus with respect to diestrus and that the content and release of these prolactin forms from Anterior Pituitary cells in culture were increased by estradiol. A recombinant preparation of 16 kDa prolactin induced apoptosis (determined by TUNEL assay and flow cytometry) of cultured Anterior Pituitary cells and lactotropes from ovariectomized rats only in the presence of estradiol, as previously reported for other proapoptotic factors in the Anterior Pituitary. In addition, 16 kDa prolactin decreased forskolin-induced proliferation (evaluated by BrdU incorporation) of rat total Anterior Pituitary cells and lactotropes in culture and decreased the proportion of cells in S-phase of the cell cycle (determined by flow cytometry). In conclusion, our study indicates that the Anterior Pituitary production of 16 kDa prolactin is variable along the estrous cycle and increased by estrogens. The antiproliferative and estradiol-dependent proapoptotic actions of this vasoinhibin may be involved in the control of Anterior Pituitary cell renewal.
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Role of Estrogens in Anterior Pituitary Gland Remodeling during the Estrous Cycle
Frontiers of hormone research, 2010Co-Authors: Sandra Zárate, Verónica Zaldivar, Daniel Pisera, Daniela Radl, Getal Jaita, L. Magri, Adriana SeilicovichAbstract:In this review, we analyze the action of estrogens leading to the remodeling of the Anterior Pituitary gland, especially during the estrous cycle. Proliferation and death of Anterior Pituitary cells a
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Cell life and death in the Anterior Pituitary gland: role of oestrogens.
Journal of neuroendocrinology, 2010Co-Authors: Adriana SeilicovichAbstract:Apoptotic processes play an important role in the maintenance of cell numbers in the Anterior Pituitary gland during physiological endocrine events. In this review, we summarise the regulation of apoptosis of Anterior Pituitary cells, particularly lactotrophs, somatotrophs and gonadotrophs, and analyse the possible mechanisms involved in oestrogen-induced apoptosis in Anterior Pituitary cells. Oestrogens exert apoptotic actions in several cell types and act as modulators of Pituitary cell renewal, sensitising cells to both mitogenic and apoptotic signals. Local synthesis of growth factors and cytokines induced by oestradiol as well as changes in phenotypic features that enhance the responsiveness of Anterior Pituitary cells to pro-apoptotic factors may account for cyclical apoptotic activity in Anterior Pituitary cells during the oestrous cycle. Considering that tissue homeostasis results from a balance between cell proliferation and death and that mechanisms involved in apoptosis are tightly regulated, defects in cell death processes could have a considerable physiopathological impact.
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Anterior Pituitary cell renewal during the estrous cycle.
Frontiers of hormone research, 2006Co-Authors: Marianela Candolfi, Verónica Zaldivar, Gabriela Jaita, Adriana SeilicovichAbstract:The Anterior Pituitary gland undergoes a process of cell renewal during the estrous cycle. Although the occurrence of proliferation and death of Anterior Pituitary cells at specific stages of the estrous cycle is well known, the underlying mechanisms that regulate these processes are still being uncovered. In spite of the recognized proliferative effects of estrogens on lactotropes, recent evidence shows that estrogens can also trigger antiproliferative and apoptotic responses in Anterior Pituitary cells. In the present review we analyze the actions of gonadal steroids on proliferation and death of Anterior Pituitary cells during the estrous cycle and the mediators involved in these actions. Estradiol sensitizes Anterior Pituitary cells not only to mitogenic stimuli but also to apoptotic signals and upregulates local synthesis of tropic growth factors as well as proapoptotic cytokines. Several growth factors and cytokines have been shown to induce estrogen-dependent lactotrope proliferation and death, whereas progesterone antagonizes estrogen-induced effects. These locally synthesized factors may mediate the effects of gonadal steroids in the process of Anterior Pituitary cell renewal during the estrous cycle.
Bartolome Burguera - One of the best experts on this subject based on the ideXlab platform.
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Leptin and Leptin Receptor in Anterior Pituitary Function
Pituitary, 2001Co-Authors: Ricardo V Lloyd, Sergio Vidal, Marta Emma Couce, Eva Horvath, Itaru Tsumanuma, Kalman Kovacs, Bernd W Scheithauer, Bartolome BurgueraAbstract:Leptin is a 16 kDa protein that exerts important effects on the regulation of food intake and energy expenditure by interacting with the leptin receptor in the brain and in many other tissues. Although leptin is produced mainly by white adipose tissue, several laboratories have shown low levels of leptin production by a growing number of tissues including the Anterior Pituitary gland. Many studies have implicated leptin in Anterior Pituitary function including the observation that homozygous mutations of the leptin receptor gene led to morbid obesity, lack of pubertal development and decreased GH and TSH secretion. In addition, leptin functions as a neuroendocrine hormone and regulates many metabolic activities. Leptin also interacts with and regulates the hypothalamic-Pituitary-adrenal, the hypothalamic-Pituitary-thyroid and the hypothalamic-Pituitary-gonadal axes. All of the Anterior Pituitary cell types express the leptin receptor. However, leptin has been localized in specific subtypes of Anterior Pituitary cells indicating cell type-specific production of leptin in the Anterior Pituitary. Subcellular localization of leptin indicates co-storage with secretory granules and implicates hypothalamic releasing hormones in leptin secretion from Anterior Pituitary hormone cells. Leptin signal transduction in the Anterior Pituitary has been shown to involve the janus protein-tyrosine kinase (JAK)/signal transducer and activation of transcription (STAT) as well as suppressor of cytokine signalling (SOCS). These proteins are activated by tyrosine-phosphorylation in Anterior Pituitary cells. The various steps in Pituitary leptin signal transduction remain to be elucidated.
Gunter K Stalla - One of the best experts on this subject based on the ideXlab platform.
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Inflammatory Mediator Action on the Anterior Pituitary Gland
The Hypothalamus-Pituitary-Adrenal Axis, 2007Co-Authors: Damiana Giacomini, Gunter K Stalla, Matias Acuña, Alberto Carbia Nagashima, Carolina Perez Castro, Marcelo Paez-pereda, Ulrich Renner, Eduardo ArztAbstract:Abstract Interleukin-1 (IL-1), IL-6, and other cytokines mainly produced by endotoxin [lipopolysaccharide (LPS)]-activated monocytes and macrophages, are known to be responsible for the acute phase and inflammatory response. These cytokines also influence the secretion of Anterior Pituitary hormones and play an important role in the interaction between the immune and the endocrine systems. Moreover, IL-1, IL-6, and their receptors are expressed and produced within the Anterior Pituitary influencing the growth and function of Pituitary cells. Thus, we propose that they act as autocrine or paracrine regulators of Pituitary homeostasis. In addition, intraPituitary production of IL-1 and IL-6 is also induced by LPS showing another link between the immune and the endocrine systems. The present review summarizes the actual knowledge about the actions of IL-1 and IL-6 (and related cytokines) known to regulate the Anterior Pituitary physiology and the involvement of LPS in modulating these intraPituitary cytokine pathways.
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Anterior Pituitary hormone abnormalities following traumatic brain injury
Journal of Neurotrauma, 2005Co-Authors: M Schneider, H J Schneider, Gunter K StallaAbstract:Traumatic brain injury (TBI) leads to approximately 100 hospitalizations per 100,000/year. Whereas diabetes insipidus is a well-known complication of TBI, Anterior hypopituitarism as a consequence of TBI has been regarded as rare. More recent studies, however, suggest a prevalence of at least 30% of Anterior Pituitary dysfunction after TBI. Clinical signs of Anterior hypopituitarism are often subtle and may be masked by sequalae of TBI. Therefore, post-traumatic Anterior Pituitary dysfunction may remain undiagnosed and, possibly, aggravate symptoms of brain injury. Moreover it may, if undiagnosed, lead to potentially fatal endocrine crises. This review updates clinical researchers, physicians, and other healthcare providers on the relationship between TBI and subsequent Anterior Pituitary insufficiency.
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Pathophysiological Role of the Cytokine Network in the Anterior Pituitary Gland
Frontiers in neuroendocrinology, 1999Co-Authors: Eduardo Arzt, Carolina Perez Castro, Ulrich Renner, Marcelo Paez Pereda, Uberto Pagotto, Gunter K StallaAbstract:Recent evidence has demonstrated that cytokines and other growth factors act in the Anterior Pituitary gland. Using the traditional criteria employed to determine autocrine or paracrine functions our review shows that, in addition to their role as lymphocyte messengers, certain cytokines are autocrine or paracrine regulators of Anterior Pituitary function and growth. The cytokines known to regulate and/or be expressed in the Anterior Pituitary include the inflammatory cytokine family (IL-1 and its endogenous antagonist, IL-1ra; TNF-α, and IL-6), the Th1-cytokines (IL-2 and IFN-γ), and other cytokines such as LIF, MIF, and TGF-β. This review examines at the cellular, molecular, and physiological levels whether: (1) each cytokine alters some aspect of Pituitary physiology; (2) receptors for the cytokine are expressed in the gland; and (3) the cytokine is produced in the Anterior Pituitary. Should physiological stimuli regulate Pituitary cytokine production, this would constitute additional proof of their autocrine/paracrine role. In this context, we analyze in this review the current literature on the actions of cytokines known to regulate Anterior Pituitary hormone secretion, selecting thein vivostudies that support the direct action of the cytokine in the Anterior Pituitary. Further support for direct regulatory action is provided byin vitrostudies, in explant cultures or Pituitary cell lines. The cytokine receptors that have been demonstrated in the Pituitary of several species are also discussed. The endogenous production of the homologous cytokines and the regulation of this expression are analyzed. The evidence indicating that cytokines also regulate the growth and proliferation of Pituitary cells is reviewed. This action is particularly important since it suggests that intrinsically produced cytokines may play a role in the pathogenesis of Pituitary adenomas. The complex cell to cell communication involved in the action of these factors is discussed.
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Cytokines: Autocrine and Paracrine Roles in the Anterior Pituitary
Neuroimmunomodulation, 1996Co-Authors: Eduardo Arzt, Gunter K StallaAbstract:In addition to their role as lymphocyte messengers, cytokines also act at the Anterior Pituitary gland as autocrine or paracrine regulators of Anterior Pituitary function. As a cellular and molecular basis for this latter role, receptors for interleukin (IL)-1, IL-2 and IL-6 have been demonstrated in the Pituitary of several species, as the endogenous production of the homologous cytokines. Additional cytokines are synthesized in or alter the function of the Pituitary. IL-1, IL-2 and IL-6 regulate not only the secretion of Pituitary hormones, but also the growth and proliferation of Pituitary cells. This latter action suggests that intrinsically produced cytokines play a role in the pathogenesis of Pituitary adenomas. Cytokines thus constitute a complex autocrine or paracrine network that contributes to the regulation of Anterior Pituitary physiology and pathophysiology.
Debra A. Schell - One of the best experts on this subject based on the ideXlab platform.
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Oxytocin and the Anterior Pituitary gland.
Advances in experimental medicine and biology, 1995Co-Authors: Willis K. Samson, Debra A. SchellAbstract:Release of oxytocin into the vicinity of the long portal vessels connecting the hypothalamus with the Anterior Pituitary gland and the presence of short portal vessels connecting the posterior lobe to the Anterior Pituitary established the potential for the peptide to act in a neuroendocrine fashion controlling the release of one or several adenohypophyseal hormones. Indeed, oxytocin receptors are present in the gland and numerous trophic effects of the peptide have been described, some with apparent physiological relevance. Thus under defined physiologic conditions a participatory role for oxytocin in the physiologic regulation of at least two hormones, prolactin and adrenocorticotropin, has been evidenced and there is developing credence to the concept that oxytocin may indirectly control gonadotroph function as well. Most recently, novel technologies have identified subpopulations of oxytocin receptive cells within a given cell type in the Anterior Pituitary gland and the concept of a modulatory effect of the nonapeptide on primary regulatory events has arisen.
Daniel Pisera - One of the best experts on this subject based on the ideXlab platform.
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Estradiol Upregulates c-FLIPlong Expression in Anterior Pituitary Cells.
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2015Co-Authors: Gabriela Jaita, Sandra Zárate, Jimena Ferraris, María Florencia Gottardo, Guadalupe Eijo, María Laura Magri, Daniel Pisera, Adriana SeilicovichAbstract:Anterior Pituitary cell turnover depends on a tight balance between proliferation and apoptosis. We have previously shown that estrogens sensitize Anterior Pituitary cells to pro-apoptotic stimuli. c-FLIP (cellular-FLICE-inhibitory-protein) isoforms are regulatory proteins of apoptosis triggered by death receptors. c-FLIPshort isoform competes with procaspase-8 inhibiting its activation. However, c-FLIPlong isoform may have a pro- or anti-apoptotic function depending on its expression level. In the present study, we explored whether estrogens modulate c-FLIP expression in Anterior Pituitary cells from ovariectomized (OVX) rats and in GH3 cells, a somatolactotrope cell line. Acute administration of 17β-estradiol to OVX rats increased c-FLIPlong expression in the Anterior Pituitary gland without changing c-FLIPshort expression as assessed by Western blot. Estradiol in vitro also increased c-FLIPlong expression in Anterior Pituitary cells but not in GH3 cells. As determined by flow cytometry, the percentage of Anterior Pituitary cells expressing c-FLIP was higher than in GH3 cells. However, c-FLIP fluorescence intensity in GH3 cells was higher than in Anterior Pituitary cells. FasL increased the percentage of TUNEL-positive GH3 cells incubated either with or without estradiol suggesting that the pro-apoptotic action of Fas activation is estrogen-independent. Our results show that unlike what happens in nontumoral Pituitary cells, estrogens do not modulate either c-FLIPlong expression or FasL-induced apoptosis in GH3 cells. The stimulatory effect of estradiol on c-FLIPlong expression could be involved in the sensitizing effect of this steroid to apoptosis in Anterior Pituitary cells. The absence of this estrogenic action in tumor Pituitary cells could be involved in their tumor-like behavior.
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N-terminal prolactin-derived fragments, vasoinhibins, are proapoptoptic and antiproliferative in the Anterior Pituitary.
PloS one, 2011Co-Authors: Jimena Ferraris, Verónica Zaldivar, Gabriela Jaita, Adriana Seilicovich, Sandra Zárate, Guadalupe Eijo, Daniela Radl, Carmen Clapp, Daniel PiseraAbstract:The Anterior Pituitary is under a constant cell turnover modulated by gonadal steroids. In the rat, an increase in the rate of apoptosis occurs at proestrus whereas a peak of proliferation takes place at estrus. At proestrus, concomitant with the maximum rate of apoptosis, a peak in circulating levels of prolactin is observed. Prolactin can be cleaved to different N-terminal fragments, vasoinhibins, which are proapoptotic and antiproliferative factors for endothelial cells. It was reported that a 16 kDa vasoinhibin is produced in the rat Anterior Pituitary by cathepsin D. In the present study we investigated the Anterior Pituitary production of N-terminal prolactin-derived fragments along the estrous cycle and the involvement of estrogens in this process. In addition, we studied the effects of a recombinant vasoinhibin, 16 kDa prolactin, on Anterior Pituitary apoptosis and proliferation. We observed by Western Blot that N-terminal prolactin-derived fragments production in the Anterior Pituitary was higher at proestrus with respect to diestrus and that the content and release of these prolactin forms from Anterior Pituitary cells in culture were increased by estradiol. A recombinant preparation of 16 kDa prolactin induced apoptosis (determined by TUNEL assay and flow cytometry) of cultured Anterior Pituitary cells and lactotropes from ovariectomized rats only in the presence of estradiol, as previously reported for other proapoptotic factors in the Anterior Pituitary. In addition, 16 kDa prolactin decreased forskolin-induced proliferation (evaluated by BrdU incorporation) of rat total Anterior Pituitary cells and lactotropes in culture and decreased the proportion of cells in S-phase of the cell cycle (determined by flow cytometry). In conclusion, our study indicates that the Anterior Pituitary production of 16 kDa prolactin is variable along the estrous cycle and increased by estrogens. The antiproliferative and estradiol-dependent proapoptotic actions of this vasoinhibin may be involved in the control of Anterior Pituitary cell renewal.
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Role of Estrogens in Anterior Pituitary Gland Remodeling during the Estrous Cycle
Frontiers of hormone research, 2010Co-Authors: Sandra Zárate, Verónica Zaldivar, Daniel Pisera, Daniela Radl, Getal Jaita, L. Magri, Adriana SeilicovichAbstract:In this review, we analyze the action of estrogens leading to the remodeling of the Anterior Pituitary gland, especially during the estrous cycle. Proliferation and death of Anterior Pituitary cells a
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Characterization of tachykinin NK2 receptor in the Anterior Pituitary gland
Life sciences, 2003Co-Authors: Daniel Pisera, Marianela Candolfi, Andrea De Laurentiis, Adriana SeilicovichAbstract:Abstract Tachykinins are a family of bioactive peptides that interact with three subtypes of receptors: NK1, NK2 and NK3. Substance P has greater affinity for NK1, and neurokinin A (NKA) for NK2 receptor subtype. Although only NK1 receptor has been characterized in the Anterior Pituitary gland, some evidence suggests the existence of NK2 receptors in this gland. Therefore, we investigated the presence of NK2 receptors in the Anterior Pituitary gland of male rats by radioligand binding studies using labeled SR48968, a non peptidic specific antagonist. [ 3 H]SR48968 specific binding to cultured Anterior Pituitary cells was time-dependent and saturable, but with a lower affinity than previously reported values for cells expressing NK2 receptors. Unlabeled NKA inhibited only partially [ 3 H]SR48968 specific binding to whole Anterior Pituitary cells. Since SR48968 is a non polar molecule, we performed experiments to discriminate surface from intracellular binding sites. SR48968 exhibited both surface and intracellular specific binding. Analysis of the surface-bound ligand indicated that [ 3 H]SR48968 binds to one class of receptor with high affinity. Neurokinin A completely displaced [ 3 H]SR48968 surface specific binding fitting to a two-site/two-state model with high and low affinity. Additionally, immunocytochemical studies showed that the NK2 receptor is expressed at least in a subset of lactotropes. These results demonstrate the presence of NK2 receptors in the Anterior Pituitary gland and suggest that NKA actions in this gland are mediated, at least in part, by the NK2 receptor subtype.