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J M Kuhn - One of the best experts on this subject based on the ideXlab platform.
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production and metabolism of serotonin 5 ht by the human adrenal cortex Paracrine Stimulation of aldosterone secretion by 5 ht
The Journal of Clinical Endocrinology and Metabolism, 2001Co-Authors: Herve Lefebvre, Patricia Compagnon, Vincent Contesse, C Delarue, Christian Thuillez, Hubert Vaudry, J M KuhnAbstract:In the human adrenal cortex, serotonin (5-HT) is contained in mast-like cells, and we have shown that 5-HT stimulates aldosterone secretion, suggesting that 5-HT may control glomerulosa cells through a Paracrine mechanism. Concurrently, the presence of 5-hydroxyindolacetic acid in human adrenocortical extracts indicates that 5-HT may be metabolized after local release by mast cells. The aim of the present study was to investigate in vitro the production and metabolism of 5-HT by the human adrenal cortex. Perifused adrenal slices released spontaneously detectable amounts of 5-HT (0.74 ± 0.38 fmol/mg wet tissue·min). The mast cell-depleting drug compound 48/80 induced a burst of 5-HT secretion followed by a gradual increase in aldosterone production. Administration of the specific 5-HT4 receptor antagonist GR 113808 (10−6 m) did not affect compound 48/80-induced 5-HT release but abolished the stimulatory effect of compound 48/80 on aldosterone secretion, indicating that 5-HT released locally is responsible ...
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production and metabolism of serotonin 5 ht by the human adrenal cortex Paracrine Stimulation of aldosterone secretion by 5 ht
The Journal of Clinical Endocrinology and Metabolism, 2001Co-Authors: Herve Lefebvre, Patricia Compagnon, Vincent Contesse, C Delarue, Christian Thuillez, Hubert Vaudry, J M KuhnAbstract:In the human adrenal cortex, serotonin (5-HT) is contained in mast-like cells, and we have shown that 5-HT stimulates aldosterone secretion, suggesting that 5-HT may control glomerulosa cells through a Paracrine mechanism. Concurrently, the presence of 5-hydroxyindolacetic acid in human adrenocortical extracts indicates that 5-HT may be metabolized after local release by mast cells. The aim of the present study was to investigate in vitro the production and metabolism of 5-HT by the human adrenal cortex. Perifused adrenal slices released spontaneously detectable amounts of 5-HT (0.74 +/- 0.38 fmol/mg wet tissue.min). The mast cell-depleting drug compound 48/80 induced a burst of 5-HT secretion followed by a gradual increase in aldosterone production. Administration of the specific 5-HT(4) receptor antagonist GR 113808 (10(-6) M) did not affect compound 48/80-induced 5-HT release but abolished the stimulatory effect of compound 48/80 on aldosterone secretion, indicating that 5-HT released locally is responsible for a Paracrine control of steroidogenesis. Incubation of cells from the human adrenal cortex with 5-HT (10(-5) M) provoked the formation of the 5-HT metabolite 5-hydroxytryptophol. The type A monoamine oxidase (MAO) inhibitor clorgyline (10(-6) M) suppressed the metabolism of 5-HT into 5-hydroxytryptophol. Immunocytochemical staining of cultured cells revealed the presence of a subpopulation of MAO-A-positive cells. Double labeling with an antiserum against chromogranin A showed that MAO-A was actually contained in chromaffin cells. Similarly, immunohistochemical staining of adrenal slices showed that MAO-A was expressed in chromaffin cells located both in the medulla and in intracortical rays. In conclusion, the present study shows that, in the human adrenal cortex, 5-HT, released by mast-cells, may stimulate aldosterone secretion in a Paracrine manner. Our data also indicate that 5-HT is metabolized by MAO-A located in intracortical chromaffin cells.
Herve Lefebvre - One of the best experts on this subject based on the ideXlab platform.
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production and metabolism of serotonin 5 ht by the human adrenal cortex Paracrine Stimulation of aldosterone secretion by 5 ht
The Journal of Clinical Endocrinology and Metabolism, 2001Co-Authors: Herve Lefebvre, Patricia Compagnon, Vincent Contesse, C Delarue, Christian Thuillez, Hubert Vaudry, J M KuhnAbstract:In the human adrenal cortex, serotonin (5-HT) is contained in mast-like cells, and we have shown that 5-HT stimulates aldosterone secretion, suggesting that 5-HT may control glomerulosa cells through a Paracrine mechanism. Concurrently, the presence of 5-hydroxyindolacetic acid in human adrenocortical extracts indicates that 5-HT may be metabolized after local release by mast cells. The aim of the present study was to investigate in vitro the production and metabolism of 5-HT by the human adrenal cortex. Perifused adrenal slices released spontaneously detectable amounts of 5-HT (0.74 ± 0.38 fmol/mg wet tissue·min). The mast cell-depleting drug compound 48/80 induced a burst of 5-HT secretion followed by a gradual increase in aldosterone production. Administration of the specific 5-HT4 receptor antagonist GR 113808 (10−6 m) did not affect compound 48/80-induced 5-HT release but abolished the stimulatory effect of compound 48/80 on aldosterone secretion, indicating that 5-HT released locally is responsible ...
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production and metabolism of serotonin 5 ht by the human adrenal cortex Paracrine Stimulation of aldosterone secretion by 5 ht
The Journal of Clinical Endocrinology and Metabolism, 2001Co-Authors: Herve Lefebvre, Patricia Compagnon, Vincent Contesse, C Delarue, Christian Thuillez, Hubert Vaudry, J M KuhnAbstract:In the human adrenal cortex, serotonin (5-HT) is contained in mast-like cells, and we have shown that 5-HT stimulates aldosterone secretion, suggesting that 5-HT may control glomerulosa cells through a Paracrine mechanism. Concurrently, the presence of 5-hydroxyindolacetic acid in human adrenocortical extracts indicates that 5-HT may be metabolized after local release by mast cells. The aim of the present study was to investigate in vitro the production and metabolism of 5-HT by the human adrenal cortex. Perifused adrenal slices released spontaneously detectable amounts of 5-HT (0.74 +/- 0.38 fmol/mg wet tissue.min). The mast cell-depleting drug compound 48/80 induced a burst of 5-HT secretion followed by a gradual increase in aldosterone production. Administration of the specific 5-HT(4) receptor antagonist GR 113808 (10(-6) M) did not affect compound 48/80-induced 5-HT release but abolished the stimulatory effect of compound 48/80 on aldosterone secretion, indicating that 5-HT released locally is responsible for a Paracrine control of steroidogenesis. Incubation of cells from the human adrenal cortex with 5-HT (10(-5) M) provoked the formation of the 5-HT metabolite 5-hydroxytryptophol. The type A monoamine oxidase (MAO) inhibitor clorgyline (10(-6) M) suppressed the metabolism of 5-HT into 5-hydroxytryptophol. Immunocytochemical staining of cultured cells revealed the presence of a subpopulation of MAO-A-positive cells. Double labeling with an antiserum against chromogranin A showed that MAO-A was actually contained in chromaffin cells. Similarly, immunohistochemical staining of adrenal slices showed that MAO-A was expressed in chromaffin cells located both in the medulla and in intracortical rays. In conclusion, the present study shows that, in the human adrenal cortex, 5-HT, released by mast-cells, may stimulate aldosterone secretion in a Paracrine manner. Our data also indicate that 5-HT is metabolized by MAO-A located in intracortical chromaffin cells.
Adhemar Longattofilho - One of the best experts on this subject based on the ideXlab platform.
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kit activation in uterine cervix adenosquamous carcinomas by kit scf autocrine Paracrine Stimulation loops
Gynecologic Oncology, 2008Co-Authors: Olga Martinho, Alberto Goncalves, Marise Amaral Reboucas Moreira, Luiz Fernando Jube Ribeiro, Geraldo Silva Queiroz, Fernando Schmitt, Rui Manuel Reis, Adhemar LongattofilhoAbstract:Abstract Objectives Uterine adenosquamous carcinoma (ASC) is an uncommon, yet, one of the most aggressive cervical cancer subtype. The successful treatment of some tumors, such as gastrointestinal stromal tumors (GISTs), by anti-KIT inhibitors fosters the study of this receptor tyrosine kinase in other malignancies. In the present study, we intended to molecularly characterize KIT in ASC. Methods In a series of 30 cases, we studied KIT (CD117), KIT phosphorylated/activated form, as well as KIT ligand, stem cell factor (SCF), by immunohistochemistry. We further screened for KIT hotspot mutations (exon 9, 11, 13 and 17) by PCR-SSCP and for KIT gene amplification by Quantitative real-time PCR in CD117 positive cases. Results We observed CD117 expression in ∼13% of cases, with ∼7% co-expressing SCF, which resulted in KIT phosphorylation/activation. No KIT activating mutations or gene amplification were found, despite the presence of 4q aneuploidy in one case. Conclusions This is the first study assessing KIT activation and molecular alterations in a large series of rare ASC. Our findings showed the absence of KIT molecular alterations and suggested the presence of KIT activation in a small proportion of cases through KIT/SCF co-expression.
E Torres - One of the best experts on this subject based on the ideXlab platform.
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leptin mediates the parathyroid hormone related protein Paracrine Stimulation of fetal lung maturation
American Journal of Physiology-lung Cellular and Molecular Physiology, 2002Co-Authors: J S Torday, Hui Sun, L Wang, E TorresAbstract:Developing rat lung lipofibroblasts express leptin beginning on embryonic day (E) 17, increasing 7- to 10-fold by E20. Leptin and its receptor are expressed mutually exclusively by fetal lung fibro...
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pre and postnatal lung development maturation and plasticity leptin mediates the parathyroid hormone related protein Paracrine Stimulation of fetal lung maturation
2002Co-Authors: J S Torday, Hui Sun, L Wang, E TorresAbstract:Torday, J. S., H. Sun, L. Wang, and E. Torres. Leptin mediates the parathyroid hormone-related protein Paracrine Stimulation of fetal lung maturation. Am J Physiol Lung Cell Mol Physiol 282: L405–L410, 2002.—Developing rat lung lipofibroblasts express leptin beginning on embryonic day (E) 17, increasing 7to 10-fold by E20. Leptin and its receptor are expressed mutually exclusively by fetal lung fibroblasts and type II cells, suggesting a Paracrine signaling “loop.” This hypothesized mechanism is supported by the following experimental data: 1) leptin stimulates the de novo synthesis of surfactant phospholipid by both fetal rat type II cells (400% 100 ng 1 ml 1 24 h 1) and adult human airway epithelial cells (85% 100 ng 1 24 h 1); 2) leptin is secreted by lipofibroblasts in amounts that stimulate type II cell surfactant phospholipid synthesis in vitro; 3) epithelial cell secretions such as parathyroid hormone-related protein (PTHrP), PGE2, and dexamethasone stimulate leptin expression by fetal rat lung fibroblasts; 4) PTHrP or leptin stimulate the de novo synthesis of surfactant phospholipid (2to 2.5-fold/24 h) and the expression of surfactant protein B (SP-B; 25-fold/24 h) by fetal rat lung explants, an effect that is blocked by a leptin antibody; and 5) a PTHrP receptor antagonist inhibits the expression of leptin mRNA by explants but does not inhibit leptin Stimulation of surfactant phospholipid or SP-B expression, indicating that PTHrP Paracrine Stimulation of type II cell maturation requires leptin expression by lipofibroblasts. This is the first demonstration of a Paracrine loop that functionally cooperates to induce alveolar acinar lung development.
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leptin mediates the parathyroid hormone related protein Paracrine Stimulation of fetal lung maturation pre and postnatal lung development maturation and plasticity
American Journal of Physiology-lung Cellular and Molecular Physiology, 2002Co-Authors: J S Torday, Hui Sun, L Wang, E TorresAbstract:Developing rat lung lipofibroblasts express leptin beginning on embryonic day (E) 17, increasing 7- to 10-fold by E20. Leptin and its receptor are expressed mutually exclusively by fetal lung fibroblasts and type II cells, suggesting a Paracrine signaling loop. This hypothesized mechanism is supported by the following experimental data: 1) leptin stimulates the de novo synthesis of surfactant phospholipid by both fetal rat type II cells (400%.100 ng -1 .ml -1 .24 h -1 ) and adult human airway epithelial cells (85%.100 ng -1 .24 h -1 ); 2) leptin is secreted by lipofibroblasts in amounts that stimulate type II cell surfactant phospholipid synthesis in vitro; 3) epithelial cell secretions such as parathyroid hormone-related protein (PTHrP), PGE 2 , and dexamethasone stimulate leptin expression by fetal rat lung fibroblasts; 4) PTHrP or leptin stimulate the de novo synthesis of surfactant phospholipid (2- to 2.5-fold/24 h) and the expression of surfactant protein B (SP-B; >25-fold/24 h) by fetal rat lung explants, an effect that is blocked by a leptin antibody; and 5) a PTHrP receptor antagonist inhibits the expression of leptin mRNA by explants but does not inhibit leptin Stimulation of surfactant phospholipid or SP-B expression, indicating that PTHrP Paracrine Stimulation of type II cell maturation requires leptin expression by lipofibroblasts. This is the first demonstration of a Paracrine loop that functionally cooperates to induce alveolar acinar lung development.
Pieter A Doevendans - One of the best experts on this subject based on the ideXlab platform.
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17β estradiol antagonizes cardiomyocyte hypertrophy by autocrine Paracrine Stimulation of a guanylyl cyclase a receptor cyclic guanosine monophosphate dependent protein kinase pathway
Circulation, 2004Co-Authors: Fawzi A Babiker, Leon J De Windt, Martin Van Eickels, Victor L Thijssen, R Bronsaer, C Grohe, Marc Van Bilsen, Pieter A DoevendansAbstract:BACKGROUND: Significant gender-related differences exist in the development of left ventricular hypertrophy (LVH). In addition, administration of 17beta-estradiol (E2) to ovariectomized female mice attenuates the development of LVH, demonstrating an antagonistic role for E2 in this process, although no molecular mechanism has been proposed for this phenomenon. METHODS AND RESULTS: E2 attenuated phenylephrine and endothelin-1 induced hypertrophy in neonatal cardiomyocytes, and E2 directly induced atrial natriuretic factor (ANF) expression as assessed by Northern blot, immunocytochemical analyses, and transient transfection assays using ANF promoter deletion fragments. Both the antihypertrophic effects and ANF induction could be blocked by the estrogen receptor antagonist ICI 182,780, which demonstrates a genomic, estrogen receptor-dependent pathway. To mimic E2-induced autocrine/Paracrine effects through Stimulation of the guanylyl cyclase A receptor (ANF receptor), cardiomyocytes were stimulated with phenylephrine or endothelin-1 in the presence of exogenous ANF or 8-bromo-cyclic guanosine monophosphate (cGMP), both of which attenuated agonist-induced hypertrophy. Both estrogen and ANF increased cGMP activity. The antihypertrophic effect of ANF could be reduced with extracellular ANF antibodies in a dose-dependent manner. cGMP-dependent protein kinase mediates the antihypertrophic effects of E2, so cardiomyocytes were agonist stimulated in the presence of the cGMP-dependent protein kinase blocker KT-5823. KT-5823 not only reversed the antihypertrophic properties of E2, ANF, or 8-bromo-cGMP, but also evoked potentiation of hypertrophy. CONCLUSIONS: E2-mediated induction of ANF in cardiac hypertrophy contributes to its antagonistic effects in LVH.
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17β estradiol antagonizes cardiomyocyte hypertrophy by autocrine Paracrine Stimulation of a guanylyl cyclase a receptor cyclic guanosine monophosphate dependent protein kinase pathway
Circulation, 2004Co-Authors: Fawzi A Babiker, Leon J De Windt, Victor L Thijssen, R Bronsaer, C Grohe, Martin Van Eickels, Marc Van Bilsen, Pieter A DoevendansAbstract:Background— Significant gender-related differences exist in the development of left ventricular hypertrophy (LVH). In addition, administration of 17β-estradiol (E2) to ovariectomized female mice attenuates the development of LVH, demonstrating an antagonistic role for E2 in this process, although no molecular mechanism has been proposed for this phenomenon. Methods and Results— E2 attenuated phenylephrine and endothelin-1 induced hypertrophy in neonatal cardiomyocytes, and E2 directly induced atrial natriuretic factor (ANF) expression as assessed by Northern blot, immunocytochemical analyses, and transient transfection assays using ANF promoter deletion fragments. Both the antihypertrophic effects and ANF induction could be blocked by the estrogen receptor antagonist ICI 182,780, which demonstrates a genomic, estrogen receptor-dependent pathway. To mimic E2-induced autocrine/Paracrine effects through Stimulation of the guanylyl cyclase A receptor (ANF receptor), cardiomyocytes were stimulated with phenyle...
