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Your search keyword '"MESH: Pituitary Adenylate Cyclase-Activating Polypeptide"' showing total 3 results
Start Over Descriptor "MESH: Pituitary Adenylate Cyclase-Activating Polypeptide" Journal journal of neurochemistry
3 results on '"MESH: Pituitary Adenylate Cyclase-Activating Polypeptide"'

1. Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates the expression and the release of tissue plasminogen activator (tPA) in neuronal cells: involvement of tPA in the neuroprotective effect of PACAP

Author

Raoult, Emilie, Roussel, Benoît Denis, Bénard, Magalie, Lefebvre, Thomas, Ravni, Aurélia, Ali, Carine, Vivien, Denis, Komuro, Hitoshi, Fournier, Alain, Vaudry, Hubert, Vaudry, David, Galas, Ludovic, Institut Fédératif de Recherches Multidisciplinaires sur les Peptides (IFRMP 23), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de Lutte Contre le Cancer Henri Becquerel Normandie Rouen (CLCC Henri Becquerel)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Université Le Havre Normandie (ULH), Normandie Université (NU)-CHU Rouen, Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS), Différenciation et communication neuronale et neuroendocrine (DC2N), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Plate-Forme de Recherche en Imagerie Cellulaire de Haute-Normandie (PRIMACEN), Normandie Université (NU)-Normandie Université (NU)-Institute for Research and Innovation in Biomedicine (IRIB), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), International Associated laboratory Samuel de Champlain, Institut National de la Recherche Scientifique [Québec] (INRS)-Université de Rouen Normandie (UNIROUEN), Sérine protéases et physiopathologie de l'unité neurovasculaire, Université de Caen Normandie (UNICAEN), Department of Neuroscience/NC30, Cleveland Clinic-Lerner Research Institute, Institut Armand Frappier (INRS-IAF), Institut National de la Recherche Scientifique [Québec] (INRS)-Réseau International des Instituts Pasteur (RIIP), and This work was supported by INSERM, the European Institute for Peptide Research (IFRMP23), the Cell Imaging Platform of Normandy (PRIMACEN), the FEDER program # 2517, the Interreg 4A TC2N project, the LARC-Neurosciences Network and the Région Haute-Normandie

Subjects
Male, endocrine system, MESH: Rats, Cell Survival, MESH: Neurons, Real-Time Polymerase Chain Reaction, PC12 Cells, Gene Expression Regulation, Enzymologic, Cell Movement, MESH: Tissue Plasminogen Activator, Cerebellum, MESH: PC12 Cells, Animals, MESH: Animals, cerebellar granule neurons, Enzyme Inhibitors, Rats, Wistar, MESH: Cell Movement, Neurons, integumentary system, MESH: Culture Media, Conditioned, MESH: Real-Time Polymerase Chain Reaction, MESH: Gene Expression Regulation, Enzymologic, MESH: Pituitary Adenylate Cyclase-Activating Polypeptide, MESH: Neuroprotective Agents, MESH: Rats, Wistar, MESH: Cerebellum, MESH: Male, Rats, Neuroprotective Agents, MESH: Cell Survival, MESH: Enzyme Inhibitors, [SDV.TOX]Life Sciences [q-bio]/Toxicology, Culture Media, Conditioned, Tissue Plasminogen Activator, Pituitary Adenylate Cyclase-Activating Polypeptide, neuroprotection, Female, MESH: Female, hormones, hormone substitutes, and hormone antagonists
Abstract

International audience; Pituitary adenylate cyclase-activating polypeptide (PACAP) and tissue plasminogen activator (tPA) play important roles in neuronal migration and survival. However, a direct link between the neurotrophic effects of PACAP and tPA has never been investigated. In this study, we show that, in PC12 cells, PACAP induced a 9.85-fold increase in tPA gene expression through activation of the protein kinase A- and protein kinase C-dependent signaling pathways. In immature cerebellar granule neurons (CGN), PACAP stimulated tPA mRNA expression and release of proteolytically active tPA. Immunocytochemical labeling revealed the presence of tPA in the cytoplasm and processes of cultured CGN. The inhibitory effect of PACAP on CGN motility was not affected by the tPA substrate plasminogen or the tPA inhibitor plasminogen activator inhibitor-1. In contrast, plasminogen activator inhibitor-1 significantly reduced the stimulatory effect of PACAP on CGN survival. Altogether, these data indicate that tPA gene expression is activated by PACAP in both tumoral and normal neuronal cells. The present study also demonstrates that PACAP stimulates the release of tPA which promotes CGN survival by a mechanism dependent of its proteolytic activity.

Published
2011
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2. Balanced effect of PACAP and FasL on granule cell death during cerebellar development: a morphological, functional and behavioural characterization

Author

Emma R. Isaac, Bruno J. Gonzalez, Delphine Burel, Ludovic Galas, Alain Fournier, Pierre Chapillon, Nancy M. Sherwood, Bénédicte Parent, Vincent Roy, Sébastien Arthaud, Hubert Vaudry, Arnaud Desfeux, Aurélie Allais, Institut Fédératif de Recherches Multidisciplinaires sur les Peptides (IFRMP 23), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de Lutte Contre le Cancer Henri Becquerel Normandie Rouen (CLCC Henri Becquerel)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Université Le Havre Normandie (ULH), Normandie Université (NU)-CHU Rouen, Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS), Institute for Research and Innovation in Biomedicine (IRIB), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Department of Biology, University of Victoria [Canada] (UVIC), Endothélium microcirculatoire cérébral et lésions du système nerveux central au cours du développement (Néovasc), Normandie Université (NU)-Normandie Université (NU)-Institute for Research and Innovation in Biomedicine (IRIB), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-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), Institut Armand Frappier (INRS-IAF), and Institut National de la Recherche Scientifique [Québec] (INRS)-Réseau International des Instituts Pasteur (RIIP)

Subjects
MESH: Cell Death, Cerebellum, Time Factors, MESH: Neurons, Biochemistry, MESH: Mice, Knockout, Fas ligand, MESH: Animals, Newborn, Mice, 0302 clinical medicine, MESH: Gene Expression Regulation, Developmental, MESH: Behavior, Animal, MESH: Caspase 3, MESH: Animals, Caspase, MESH: Cell Size, MESH: Bromodeoxyuridine, Mice, Knockout, Neurons, 0303 health sciences, MESH: Muscle, Skeletal, MESH: Statistics, Nonparametric, biology, Behavior, Animal, Cell Death, Caspase 3, Gene Expression Regulation, Developmental, MESH: Motor Activity, Pituitary adenylate cyclase-activating peptide, medicine.anatomical_structure, [SDV.TOX]Life Sciences [q-bio]/Toxicology, Pituitary Adenylate Cyclase-Activating Polypeptide, hormones, hormone substitutes, and hormone antagonists, medicine.medical_specialty, Programmed cell death, endocrine system, Fas Ligand Protein, MESH: Reflex, MESH: Psychomotor Performance, In Vitro Techniques, Motor Activity, Statistics, Nonparametric, 03 medical and health sciences, Cellular and Molecular Neuroscience, MESH: Mice, Inbred C57BL, Internal medicine, MESH: Cell Proliferation, Reflex, medicine, Animals, RNA, Messenger, Muscle, Skeletal, MESH: Mice, 030304 developmental biology, MESH: RNA, Messenger, Cell Proliferation, Cell Size, MESH: Pituitary Adenylate Cyclase-Activating Polypeptide, MESH: Time Factors, Granule cell, MESH: Cerebellum, MESH: Fas Ligand Protein, Mice, Inbred C57BL, Endocrinology, Animals, Newborn, Bromodeoxyuridine, Apoptosis, biology.protein, 030217 neurology & neurosurgery, Psychomotor Performance
Abstract

International audience; It is now established that the development of the CNS requires equilibrium between cell survival and apoptosis. Pituitary adenylate cyclase-activating polypeptide (PACAP) exerts a powerful protective effect on cerebellar granule cells by inhibiting the caspase 3. In contrast, Fas ligand (FasL) plays an essential role during ontogenesis in eliminating supernumerary neurons by apoptosis. To determine if PACAP and FasL interact during cerebellar development, we characterized the effects of these factors on cerebellar morphogenesis and caspase 3 activity in PACAP+/+ and PACAP-/- mice. First, we demonstrated in vivo that PACAP is able to reverse the diminution of internal granule cell layer thickness induced by FasL in PACAP+/+ and PACAP-/- mice. Second, ex vivo and immunohistochemical studies revealed that interaction between FasL and PACAP occurs through the caspase 3 activity. Third, behavioural study showed a significant difference for the PACAP + FasL group in the righting reflex test at P8 which does not persist at P60. Finally, a time course study revealed that the pro-apoptotic effect of FasL characterized at P8 was followed by a progressive compensatory mechanism in caspase 3 activity and bromodeoxyuridine incorporation. These data suggest that PACAP and FasL interact during cerebellar development to control apoptosis of granule cells and may affect some motor cerebellar functions.

Published
2010
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3. Opposite regulation of the mitochondrial apoptotic pathway by C2-ceramide and PACAP through a MAP-kinase-dependent mechanism in cerebellar granule cells

Author

Falluel-Morel, Anthony, Aubert, Nicolas, Vaudry, David, Basille, Magali, Fontaine, Marc, Fournier, Alain, Vaudry, Hubert, Gonzalez, Bruno J, Neuroendocrinologie cellulaire et moléculaire, Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratory of Defense Proteins in Immune and Inflammatory Responses, Institut National de la Santé et de la Recherche Médicale (INSERM)-Faculty of Medicine and Pharmacy-European Institute for Peptide Research-Institut Fédératif de Recherches Multidisciplinaires sur les Peptides (IFRMP 23), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de Lutte Contre le Cancer Henri Becquerel Normandie Rouen (CLCC Henri Becquerel)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Université Le Havre Normandie (ULH), Normandie Université (NU)-CHU Rouen, Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de Lutte Contre le Cancer Henri Becquerel Normandie Rouen (CLCC Henri Becquerel)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS), Institut Armand Frappier (INRS-IAF), Institut National de la Recherche Scientifique [Québec] (INRS)-Réseau International des Instituts Pasteur (RIIP), and This research was supported by an INSERM Grant (U413) and an IREB Grant (2001/22). AFM is recipient of a fellowship from the Conseil Re ́gional de Haute-Normandie (LARC-Neuroscience net- work). NA is a recipient of a fellowship from the Conseil Régional de Haute-Normandie and the CIT-IFM Recherche.

Subjects
MESH: Signal Transduction, Time Factors, MAP Kinase Kinase 4, MESH: Drug Interactions, MESH: Neurons, Fluorescent Antibody Technique, MESH: Neurotransmitter Agents, MESH: Neuropeptides, MESH: Caspase 9, MESH: Animals, Newborn, MESH: Dose-Response Relationship, Drug, Membrane Potentials, Mice, Cytosol, MESH: Cytosol, Sphingosine, MESH: Reverse Transcriptase Polymerase Chain Reaction, Cerebellum, MESH: Caspase 3, MESH: Animals, Drug Interactions, Enzyme Inhibitors, MESH: Fluorescent Antibody Technique, Cells, Cultured, bcl-2-Associated X Protein, Neurons, Neurotransmitter Agents, Caspase 3, Reverse Transcriptase Polymerase Chain Reaction, Intracellular Signaling Peptides and Proteins, Cytochromes c, MESH: Cytochromes c, Carbocyanines, MESH: Gene Expression Regulation, Caspase 9, Mitochondria, ERK, Proto-Oncogene Proteins c-bcl-2, MESH: Enzyme Inhibitors, [SDV.TOX]Life Sciences [q-bio]/Toxicology, Caspases, Pituitary Adenylate Cyclase-Activating Polypeptide, MESH: Carbocyanines, MESH: Sphingosine, Mitogen-Activated Protein Kinases, hormones, hormone substitutes, and hormone antagonists, MESH: MAP Kinase Kinase 4, MESH: Cells, Cultured, Signal Transduction, endocrine system, MESH: Rats, MESH: Mitochondria, Blotting, Western, Models, Neurological, MESH: Mitogen-Activated Protein Kinase Kinases, mitochondrial apoptotic pathway, MESH: Models, Neurological, MESH: Intracellular Signaling Peptides and Proteins, MESH: Membrane Potentials, MESH: Blotting, Western, Animals, Bcl-2, MESH: bcl-2-Associated X Protein, Nerve Growth Factors, RNA, Messenger, Rats, Wistar, MESH: Mice, MESH: RNA, Messenger, Mitogen-Activated Protein Kinase Kinases, MESH: Caspases, Dose-Response Relationship, Drug, MESH: Nerve Growth Factors, MESH: Pituitary Adenylate Cyclase-Activating Polypeptide, MESH: Time Factors, Neuropeptides, JNK Mitogen-Activated Protein Kinases, MESH: JNK Mitogen-Activated Protein Kinases, MESH: Rats, Wistar, MESH: Mitogen-Activated Protein Kinases, MESH: Cerebellum, Rats, MESH: Proto-Oncogene Proteins c-bcl-2, Animals, Newborn, Gene Expression Regulation, Bax, Benzimidazoles, JNK, MESH: Benzimidazoles
Abstract

International audience; The sphingomyelin-derived messenger ceramides provoke neuronal apoptosis through caspase-3 activation, while the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) promotes neuronal survival and inhibits caspase-3 activity. However, the mechanisms leading to the opposite regulation of caspase-3 by C2-ceramide and PACAP are currently unknown. Here, we show that PACAP prevents C2-ceramide-induced inhibition of mitochondrial potential and C2-ceramide-evoked cytochrome c release. C2-ceramide stimulated Bax expression, but had no effect on Bcl-2, while PACAP abrogated the action of C2-ceramide on Bax and stimulated Bcl-2 expression. The effects of C2-ceramide and PACAP on Bax and Bcl-2 were blocked, respectively, by the JNK inhibitor L-JNKI1 and the MEK inhibitor U0126. L-JNKI1 prevented the alteration of mitochondria induced by C2-ceramide while U0126 suppressed the protective effect of PACAP against the deleterious action of C2-ceramide on mitochondrial potential. Moreover, L-JNKI1 inhibited the stimulatory effect of C2-ceramide on caspase-9 and -3 and prevented C2-ceramide-induced cell death. U0126 blocked PACAP-induced Bcl-2 expression, abrogated the inhibitory effect of PACAP on ceramide-induced caspase-9 activity, and promoted granule cell death. The present study reveals that C2-ceramide and PACAP exert opposite effects on Bax and Bcl-2 through, respectively, JNK- and ERK-dependent mechanisms. These data indicate that the mitochondrial pathway plays a pivotal role in the pro- and anti-apoptotic effects of C2-ceramide and PACAP.

Published
2004
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