Search

Your search keyword '"MESH : Pituitary Gland"' showing total 3 results
Start Over Descriptor "MESH : Pituitary Gland"
3 results on '"MESH : Pituitary Gland"'

1. Truncation of PITX2 differentially affects its activity on physiological targets

Author

Véronique Vieira, Maurice Menasche, James P. Herman, Thierry Brue, Alain Enjalbert, Marc Abitbol, Marie-Helene Quentien, Jean-Louis Dufier, Centre de recherche en neurobiologie - neurophysiologie de Marseille (CRN2M), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de recherche thérapeutique en ophtalmologie, Université Paris Descartes - Paris 5 (UPD5)-EA2502, EA no 2502 du ministère de la Recherche, de l'Enseignement Supérieur et la Technologie, Université Paris Descartes - Paris 5 (UPD5)-CERTO, Service d'ophtalmologie [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Necker - Enfants Malades [AP-HP], Centre d'étude et de recherche thérapeutiques en ophtalmologie, Université Paris Descartes - Paris 5 (UPD5), Aix Marseille Université (AMU) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5) - EA2502, Université Paris Descartes - Paris 5 (UPD5) - CERTO, Assistance publique - Hôpitaux de Paris (AP-HP) - CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Necker - Enfants Malades [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
MESH : Cell Line, MESH : Transcription Factors, MESH : Transcription Factor Pit-1, Mutant, Electrophoretic Mobility Shift Assay, MESH : Blotting, Western, MESH : Promoter Regions, Genetic, medicine.disease_cause, MESH : Pituitary Gland, 0302 clinical medicine, Endocrinology, MESH : Prolactin, MESH: Pituitary Gland, MESH: Human Growth Hormone, MESH: Animals, MESH : Transcriptional Activation, MESH : Homeodomain Proteins, Eye Abnormalities, Promoter Regions, Genetic, 0303 health sciences, Mutation, MESH: Anterior Eye Segment, Human Growth Hormone, Eye Diseases, Hereditary, MESH: Transcription Factors, Transfection, MESH: Eye Abnormalities, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], Cell biology, MESH : Electrophoretic Mobility Shift Assay, Pituitary Gland, MESH : Mutation, Transcription Factor Pit-1, hormones, hormone substitutes, and hormone antagonists, Transcriptional Activation, congenital, hereditary, and neonatal diseases and abnormalities, medicine.medical_specialty, MESH: Mutation, Blotting, Western, MESH: Prolactin, Biology, MESH : Anterior Eye Segment, Cell Line, [SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], 03 medical and health sciences, stomatognathic system, Anterior Eye Segment, Internal medicine, MESH : Eye Abnormalities, MESH: Promoter Regions, Genetic, MESH: Homeodomain Proteins, medicine, MESH: Blotting, Western, Animals, Humans, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], MESH : Human Growth Hormone, Molecular Biology, Transcription factor, Gene, 030304 developmental biology, Homeodomain Proteins, Reporter gene, MESH: Humans, POU domain, MESH : Humans, Promoter, MESH: Cell Line, Prolactin, stomatognathic diseases, MESH: Electrophoretic Mobility Shift Assay, 030221 ophthalmology & optometry, MESH: Transcriptional Activation, MESH : Animals, sense organs, MESH: Transcription Factor Pit-1, Transcription Factors
Abstract

International audience; The bicoid-like transcription factor PITX2 has been previously described to interact with the pituitary-specific POU homeodomain factor POU1F1 (human ortholog of PIT-1) to achieve cell-specific expression of prolactin (PRL) and GH in pituitary somatolactotroph cells. In this work, we have investigated the functional properties of three PITX2 mutants reported in Axenfeld-Rieger syndrome patients relative to the regulation of these genes, using reporter genes under the control of human PRL (hPRL), hGH, or POU1F1 promoters transfected in nonpituitary and pituitary cell lines. Among the three mutations studied, Y167X and E101X introduce a premature stop codon, and F104L leads to an amino acid substitution. While PITX2(E101X) is not expressed in the cells following transfection, and PITX2(F104L) is functionally inactive, the PITX2(Y167X) mutant keeps its DNA-binding capacity and displays a markedly enhanced activation of the hPRL and POU1F1 promoters, but not of the hGH promoter. Y167X is the first mutation of PITX2 described to result in a differential effect on the activation of its different physiological targets, hPRL and POU1F1 on one hand and hGH on the other hand. The differential effect of the Y167X mutation might be linked to an interaction of PITX2 with different transcription factors or cofactors when bound to the hPRL and POU1F1 or the hGH promoters. These results might form the basis for the identification of the PITX2 protein complex necessary for the differential GH or PRL expression.

Published
2010
Full Text
View/download PDF

2. Pituitary stalk interruption syndrome in 83 patients: novel HESX1 mutation and severe hormonal prognosis in malformative forms

Author

Raja Brauner, Jean Gaudart, Gilbert Simonin, Thierry Brue, Emilie Carmona, Frédérique Albarel, Anne Barlier, Nourredine Kaffel, Frederic Castinetti, Alain Enjalbert, P. Lecomte, Alexandru Saveanu, Rachel Reynaud, Centre de recherche en neurobiologie - neurophysiologie de Marseille (CRN2M), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5), Méthodes Algorithmes pour l'Ordonnancement et les Réseaux (MAORE), Laboratoire d'Informatique de Robotique et de Microélectronique de Montpellier (LIRMM), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Laboratoire d'Enseignement et de Recherche sur le Traitement de l'Information Médicale (LERTIM), Université de la Méditerranée - Aix-Marseille 2, Centre de recherche en neurobiologie - neurophysiologie de Marseille ( CRN2M ), Aix Marseille Université ( AMU ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Université Paris Descartes - Paris 5 ( UPD5 ), Méthodes Algorithmes pour l'Ordonnancement et les Réseaux ( MAORE ), Laboratoire d'Informatique de Robotique et de Microélectronique de Montpellier ( LIRMM ), Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ) -Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Laboratoire d'Enseignement et de Recherche sur le Traitement de l'Information Médicale ( LERTIM ), Methods, Algorithms for Operations REsearch (MAORE), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Male, MESH : Transcription Factors, Endocrinology, Diabetes and Metabolism, Pedigree chart, Hypopituitarism, MESH : Child, Preschool, medicine.disease_cause, MESH : Pituitary Gland, MESH: Magnetic Resonance Imaging, 0302 clinical medicine, Endocrinology, [ SDV.BBM.BC ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], MESH : Child, MESH: Otx Transcription Factors, MESH: Pituitary Gland, MESH: SOXB1 Transcription Factors, MESH: Child, MESH : Female, MESH : Homeodomain Proteins, Child, 0303 health sciences, education.field_of_study, Mutation, Otx Transcription Factors, MESH : Otx Transcription Factors, MESH : SOXB1 Transcription Factors, Incidence (epidemiology), MESH : Infant, General Medicine, MESH: Transcription Factors, Magnetic Resonance Imaging, MESH: Infant, Ectopic Posterior Pituitary, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], medicine.anatomical_structure, Child, Preschool, Pituitary Gland, Cohort, Female, MESH : Mutation, medicine.medical_specialty, MESH: Mutation, Adolescent, MESH : Male, LIM-Homeodomain Proteins, Population, 030209 endocrinology & metabolism, Biology, 03 medical and health sciences, Posterior pituitary, Internal medicine, MESH : Adolescent, MESH : Magnetic Resonance Imaging, MESH: Homeodomain Proteins, medicine, Humans, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], education, 030304 developmental biology, Homeodomain Proteins, MESH: Adolescent, MESH: Humans, SOXB1 Transcription Factors, MESH : Humans, MESH: Child, Preschool, Infant, medicine.disease, MESH: Male, MESH: Female, Transcription Factors
Abstract

BackgroundPituitary stalk interruption syndrome (PSIS) is a particular entity in the population of patients with hypopituitarism. Only rare cases have a known genetic cause.Objectivesi) To compare subgroups with or without extra-pituitary malformations (EPM) in a cohort of PSIS patients to identify predictive factors of evolution, ii) to determine the incidence of mutations of the known pituitary transcription factor genes in PSIS.Study designWe analyzed features of 83 PSIS patients from 80 pedigrees and screened HESX1, LHX4, OTX2, and SOX3 genes.ResultsPSIS had a male predominance and was rarely familial (5%). Pituitary hypoplasia was observed only in the group with EPM. Multiple hormone deficits were observed significantly more often with versus without EPM (87.5 vs 69.5% respectively). Posterior pituitary location along the stalk was a significant protective factor regarding severity of hormonal phenotype. A novel HESX1 causative mutation was found in a consanguineous family, and two LHX4 mutations were present in familial PSIS.ConclusionPSIS patients with EPM had a more severe hormonal disorder and pituitary imaging status, suggesting an antenatal origin. HESX1 or LHX4 mutations accounted for

Published
2011
Full Text
View/download PDF

3. Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

Author

Marie-Thérèse Bluet-Pajot, Rodrigo Alvear-Perez, Philippe Zizzari, Catherine Llorens-Cortes, Annabelle Réaux-Le Goazigo, Jacques Epelbaum, Neuropeptides centraux et régulations hydrique et cardiovasculaire, Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Labex MemoLife, Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neurobiologie de la Croissance et de la Senescence, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre interdisciplinaire de recherche en biologie (CIRB), École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Labex MemoLife, Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Collège de France ( CdF ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), and Llorens Cortes, Catherine

Subjects
Male, Pituitary gland, Endocrinology, Diabetes and Metabolism, MESH: Amino Acid Sequence, MESH: Receptors, G-Protein-Coupled, MESH: Base Sequence, MESH : Tissue Distribution, Receptors, G-Protein-Coupled, Rats, Sprague-Dawley, 0302 clinical medicine, MESH: Cricetulus, MESH: Pituitary Gland, MESH: Ligands, MESH : CHO Cells, Tissue Distribution, MESH: Animals, MESH: Peptide Fragments, MESH : Ligands, 0303 health sciences, MESH : Amino Acid Sequence, MESH : Cyclic AMP, MESH: Pituitary Gland, Anterior, MESH : Cricetinae, MESH : Protein Binding, [ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, [SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Apelin, MESH : Adrenocorticotropic Hormone, Intercellular Signaling Peptides and Proteins, MESH : Carrier Proteins, medicine.medical_specialty, endocrine system, MESH : Cell Membrane, MESH : Cricetulus, MESH: Carrier Proteins, Adrenocorticotropic hormone, 03 medical and health sciences, Adrenocorticotropic Hormone, Anterior pituitary, Pituitary Gland, Anterior, MESH: CHO Cells, Physiology (medical), MESH: Protein Binding, MESH: Tissue Distribution, MESH: Adrenocorticotropic Hormone, MESH: Humans, MESH: Molecular Sequence Data, MESH : Humans, Peptide Fragments, Endocrinology, Carrier Proteins, 030217 neurology & neurosurgery, MESH : Molecular Sequence Data, Physiology, MESH: Corticotrophs, MESH: Cricetinae, MESH : Models, Biological, MESH: Rats, Sprague-Dawley, Rats, Inbred WKY, MESH : Pituitary Gland, Receptor, Corticotrophs, Cellular localization, MESH: Cyclic AMP, [SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism, Apelin Receptors, MESH : Rats, MESH : Forskolin, medicine.anatomical_structure, MESH: Pituitary Hormones, Anterior, MESH: Calcium, MESH : Receptors, G-Protein-Coupled, MESH : Transfection, MESH: Forskolin, hormones, hormone substitutes, and hormone antagonists, MESH: Rats, Inbred WKY, Endocrine gland, MESH: Rats, MESH : Male, MESH : Rats, Inbred WKY, Biology, Models, Biological, MESH : Pituitary Hormones, Anterior, MESH : Pituitary Gland, Anterior, Pituitary Hormones, Anterior, Internal medicine, medicine, Animals, MESH : Calcium, 030304 developmental biology, Apelin receptor, MESH: Transfection, MESH : Peptide Fragments, MESH: Models, Biological, MESH : Corticotrophs, MESH : Rats, Sprague-Dawley, MESH: Male, Rats, MESH : Peptide Hormones, MESH: Peptide Hormones, MESH : Base Sequence, MESH : Animals, MESH: Cell Membrane
Abstract

Apelin is a bioactive peptide recently identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ. The presence of apelin-immunoreactive nerve fibers, together with the detection of apelin receptor mRNA in the parvocellular part of the paraventricular nucleus and the stimulatory action of apelin on corticotropin-releasing hormone release, indicate that apelin modulates adrenocorticotropin (ACTH) release via an indirect action on the hypothalamus. However, a direct action of apelin in the anterior pituitary cannot be excluded. Here, we provided evidence for the existence of an apelinergic system within the adult male rat pituitary gland. Double immunofluorescence staining indicated that apelin is highly coexpressed in the anterior pituitary, mainly in corticotrophs (96.5 ± 0.3%) and to a much lower extent in somatotropes (3.2 ± 0.2%). Using in situ hybridization combined with immunohistochemistry, a high expression of apelin receptor mRNA was also found in corticotrophs, suggesting a local interaction between apelin and ACTH. In an ex vivo perifusion system of anterior pituitaries, apelin 17 (K17F, 10−6M) significantly increased basal ACTH release by 41%, whereas apelin 10 (R10F, 10−6M), an inactive apelin fragment, was ineffective. In addition, K17F but not R10F induced a dose-dependent increase in K+-evoked ACTH release, with maximal increase being observed for a 10−6M concentration. Taken together, these data outline the potential role of apelin as an autocrine/paracrine-acting peptide on ACTH release and provide morphological and neuroendocrine basis for further studies that explore the physiological role of apelin in the regulation of anterior pituitary functions.

Published
2007
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results