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9 results on '"Evanthia Mergia"'

1. Abstracts from the 8th International Conference on cGMP Generators, Effectors and Therapeutic Implications

Author

Fritz G. Rathjen, Timothy D. Calamaras, Hong Wang, Motofumi Kumazoe, Sarah Helena Nies, Jerid W. Robinson, Andreas Friebe, Balázs Tamás Németh, Michel Negrerie, Kjetil W. Andressen, Clara D. Ledsky, Sivakanan Loganathan, Kerstin Jurk, Barbara Voussen, Julia Gorelik, Mi Kyung Chang, Johannes-Peter Stasch, Friederike Cuello, Nicholas C. Blixt, S. A. Dames, Nazareno Paolocci, Gzona Bajraktari, Katherine C. Hall, Markus Waldeck-Weiermair, Marcel A. Krüger, Antonius C.F. Gorren, Donté A. Stevens, Daniel Bloch, Deborah M. Dickey, Maria Hernandez-Valladares, Lan Zhao, Alex Vincent, Jenna Scotcher, Andrzej Weichsel, Tamás Radovits, Jeremy Richman, Sophie Schobesberger, Stavros Topouzis, Regine Mühlfriedel, Dennis Busse, Reiner Frey, Sean P. Parsons, René P. Zahedi, Evanthia Mergia, Mathias W. Seeliger, Angela McLaughlin, Sylvia Nikkho, Fernando Ferreira Costa, Pavel Jansa, Ornella Manfra, Wilson A. Ferreira, Inmaculada Silos-Santiago, B. Selin Kenet, Marc Humbert, Garyfalia Makrynitsa, Katja Stehfest, Lise Román Moltzau, Shiliang Li, Chris Sarko, Lincoln R. Potter, Yusu Gu, Scott A. Waldman, Nicole Eichert, David Kilpatrick, Roland Malli, Jun Hino, Robert Solinga, Banumathi Sankaran, William R. Montfort, Alexander Kollau, Julia Davydova, Andriana Stamopoulou, Olena Rudyk, Johanna Weiss, Kenji Kangawa, Arno Fritsch, Meinrad Gawaz, Peter Sandner, Robert M. Blanton, Friedrich Grimminger, Laurinda Jaffe, Atsuko Okamoto, Elke Butt, Stefanie Peters, Christine E. Gee, Ronald J. Holewinski, Zhi Cheng Jing, Andrea Gerling, Mika Takai, Alexander Froese, Hiroshi Hosoda, Mara Goetz, Yasutake Tanaka, Ioannis I. Alexandropoulos, Amie J Moyes, Hyazinth Dobrowinski, Michael J. Shipston, Ulrike Scheib, Stefan W. Hell, Oleksandra Prysyazhna, Lukas Rüttiger, Dieter Groneberg, Vu Thao-Vi Dao, Ulrich Walter, Hariharan Subramanian, Roger Flores-Costa, Richard C. Page, Joerg Reinders, Huaqun Zhang, Dianna M. Milewicz, Martin Thunemann, Albert T. Profy, Chieri Takeuchi, Andrew B. Tobin, Darren E. Casteel, Sarah Jacobson, Philip Eaton, Cor de Witt, Nadine Mauro, Mark Aronovitz, Sevil Korkmaz-Icöz, Barbara Wilhelm, Angelos Vachaviolos, Kim Tang, Axel Gödecke, Christian Meier, Carine M. Boustany, Daniel P. Zimmer, Bernd J. Pichler, Adrian J. Hobbs, Marianne Bjørnerem, Wolfgang F. Graier, Selene J. Sollie, Jenny Tobin, Jürgen Burhenne, Meinoshin Okumura, Nancy D. Dalton, Matthias Karck, Ernst-Martin Füchtbauer, Karoline Dröbner, Kristen M. Kokkonen, Flavia Menezes, Heribert Schunkert, Kirk L. Peterson, Ying-Ju Sung, Georgios A. Spyroulias, Olga N. Petrova, Frank Eitner, Mark G. Currie, Choel Kim, Ulrike Zimmermann, Steven S. Pullen, Shunhui Zhuang, Camila B. Almeida, Sylvie Bernier, M. Wittwer, Steffen Wolter, Stylianos Michalakis, Ralf Kühn, Sara S. O. Saad, Catherine Mansfield, Joon Jung, Jennifer E. Van Eyk, Navin K. Kapur, Renate B. Pilz, David Langleben, Diane Wong, Sylvie G. Bernier, Leia C. Shuhaibar, Heinz G. Körschen, César Ibarra-Alvarado, Courtney Shea, Ryan M. Fryer, Corina Russwurm, Gilbert W. Kim, Gerald Wölkart, Marius M. Hoeper, Astrid Weiss, Harald F. Langer, Ibrahim J. Domian, Lars I. Leichert, Bernd Wissinger, Paul Allan Renhowe, Richard H. Karas, Masayuki Sasaki, Finn Olav Levy, Cor de Wit, Sonia Donzelli, Michael Russwurm, Eberhart Zrenner, Reshma S. Baliga, Holly Clifford, Jonathan C. Schisler, Cheng-Yu Chen, Nicola Conran, Jens Schlossmann, Vikas Kapil, Pablo Colorado, Boris Tchernychev, Isabelle Lamarre, Katrin Reimann, Francheska Colon-Gonzalez, Ralph T. Schermuly, Hans-Ulrich Häring, Vineet Agrawal, Peter Germano, Bernd Mayer, Katharina Beck, Moritz Lehners, Sara Vandenwijngaert, Fabíola Z. Mónica, Pavel I. Nedvetsky, Kimberly Kafadar Long, Silja Meier, Paul A. Corris, Takeshi Tokudome, Shatanik Mukherjee, Joseph R. Burgoyne, Martin Deile, Jan Giesen, Ferid Murad, G. Todd Milne, Shinpei Kawaoka, Koichi Miura, Jessica A. Wales, David A. Kass, Doris Koesling, Hongxing Chen, Frode S. Berven, Jeong Joo Kim, Friedrich W. Herberg, Kristin Hartmann, Martin Biel, Raymond L. Benza, Monte S. Willis, Daniela Bertinetti, Jaime L. Masferrer, Stefan Z. Lutz, Guang-Rong Wang, Peter Ruth, Viacheslav O. Nikolaev, Tobias Peters, Karl Ulrich Bartz-Schmidt, Arnab Ghosh, Lai Wen, Mai Kadomatsu, Sandy M. Chu, Yutaka Suzuki, Marcus Olbrich, Yigao Huang, Tobias Bauch, Thorsten Kessler, Amrita Ahluwalia, Robert Feil, Daniel Richards, Hu Sheng Qian, M Currie, Christopher Newton-Cheh, V. Kaila, Liying Qin, Peter Hegemann, Peter Wright, G-Yoon Jamie Im, Hirofumi Tachibana, Kjestine Schmidt, Pamela L. Brito, Alisa Kamynina, James C. Campbell, Adam E. Snook, Fabian Schwiering, Martin Floor, Jordi Villà-Freixa, Jana Wobst, Alexandre Dumoulin, Ali R. Banijamali, Csaba Mátyás, Harald H.H.W. Schmidt, Susanne Kohl, Mark J. Ranek, Manuela Zaccolo, Robert Lukowski, Robert Naeije, Peter P. Rainer, Stephan Rosenkranz, Emmanuel S. Buys, Simone Romoli, Andreas Papapetropoulos, Kim C. Mansky, James Wakefield, Kálmán Benke, Takashi Nojiri, Aikaterini I. Argyriou, Dongjian Hu, Glenn A. Reinhart, Cornelia Virus, Marius Ueffing, Marlies Knipper, Gerhard Hannig, Kanako Takamatsu, Athanassios Giannis, Miki Arai, Stepan Gambaryan, James E. Sheppeck, Mathew M. Mannion, S. Bruce King, Henriette Andresen, Min Zhang, Jan D. Huizinga, Jeanette Erdmann, Matthias Broser, Astrid Schrammel, Dante J. Merlino, Hossein Ardeschir Ghofrani, Gaia Calamera, Obiajulu Agha, Kathleen A Lincoln, Gerburg K. Schwaerzer, Gordon L. Warren, Andrea Neubauer, Claire Poulet, Nicoletta C. Surdo, Attila Oláh, Damian Brockschnieder, Emrah Eroglu, Carla Fernanda Franco Penteado, Walter E. Haefeli, Mihály Ruppert, Ekkehard Grünig, Konstantina Stathopoulou, Elena Walter, Gérald Simonneau, Béla Merkely, Andreas Güldner, J Keppler, Katharina Frank, Renee Sarno, Sandra Frankenreiter, Sian E. Harding, Dorit Möhrle, Paul C. Harrison, Péter Hegedűs, Hyun-Soon Geisler, James R. Klinger, Markus Wolters, Philipp Henning, Jieru E. Lin, Erik S. Blomain, Alessandro Cataliotti, Ditta Zobor, Mikiya Miyazato, Marissa Opelt, Christian Schön, John Fassett, Yue Dai, Q. Luo, Thomas G. Oertner, Linda Breci, Robert A Baumgartner, Shun Hiroi, Ping Zhang, Albert Smolenski, Paul S. Frenette, Mahmood M. Alam, Jeremy R. Egbert, Dennis J. Stuehr, Eugen Franz, Hanan Chweih, Dong I. Lee, Nadja I. Bork, Guang Liu, Hannes Schmidt, Ka Bian, Annemarie Aue, Christian Dees, Edward Seto, Manuela Harloff, Michael Paolillo Hannes Schmidt, Susanne Feil, Susanne Krasemann, Andrea Hembre Ulsund, Marina Bantzi, Laurinda A. Jaffe, Luis Agulló, Dominik M. Fischer, Wendy Baur, Kjetil Wessel Andressen, Saurav Misra, Gábor Szabó, and Oliver Pagel

Subjects
0301 basic medicine, Pharmacology, 03 medical and health sciences, 030104 developmental biology, business.industry, Pharmacology toxicology, MEDLINE, Medicine, Pharmacology (medical), business
Published
2017
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2. NO regulates the strength of synaptic inputs onto hippocampal CA1 neurons via NO-GC1/cGMP signalling

Author

Angela Neitz, Doris Koesling, Evanthia Mergia, Ute Neubacher, and Thomas Mittmann

Subjects
Male, Interneuron, Physiology, Clinical Biochemistry, Gating, Hippocampal formation, Biology, Neurotransmission, Nitric Oxide, Inhibitory postsynaptic potential, Mice, Glutamatergic, Interneurons, Physiology (medical), medicine, Animals, CA1 Region, Hippocampal, Cyclic GMP, gamma-Aminobutyric Acid, Excitatory Postsynaptic Potentials, Mice, Inbred C57BL, medicine.anatomical_structure, Inhibitory Postsynaptic Potentials, nervous system, Guanylate Cyclase, Excitatory postsynaptic potential, GABAergic, Neuroscience
Abstract

GABAergic interneurons are the predominant source of inhibition in the brain that coordinate the level of excitation and synchronization in neuronal circuitries. However, the underlying cellular mechanisms are still not fully understood. Here we report nitric oxide (NO)/NO-GC1 signalling as an important regulatory mechanism of GABAergic and glutamatergic synaptic transmission in the hippocampal CA1 region. Deletion of the NO receptor NO-GC1 induced functional alterations, indicated by a strong reduction of spontaneous and evoked inhibitory postsynaptic currents (IPSCs), which could be compensated by application of the missing second messenger cGMP. Moreover, we found a general impairment in the strength of inhibitory and excitatory synaptic inputs onto CA1 pyramidal neurons deriving from NO-GC1KO mice. Finally, we disclosed one subpopulation of GABAergic interneurons, fast-spiking interneurons, that receive less excitatory synaptic input and consequently respond with less spike output after blockage of the NO/cGMP signalling pathway. On the basis of these and previous findings, we propose NO-GC1 as the major NO receptor which transduces the NO signal into cGMP at presynaptic terminals of different neuronal subtypes in the hippocampal CA1 region. Furthermore, we suggest NO-GC1-mediated cGMP signalling as a mechanism which regulates the strength of synaptic transmission, hence being important in gating information processing between hippocampal CA3 and CA1 region.

Published
2014
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3. Differential role of NO-sensitive guanylyl cyclase isoforms NO-GC1 and NO-GC2 in auditory function in adult mice

Author

Steffen Wolter, Lukas Rüttiger, Evanthia Mergia, Nicole Eichert, Andreas Friebe, Dorit Möhrle, Marlies Knipper, and Doris Koesling

Subjects
Pharmacology, Gene isoform, endocrine system, medicine.medical_specialty, Absolute threshold of hearing, Otoacoustic emission, Guanosine, chemistry.chemical_compound, Auditory brainstem response, medicine.anatomical_structure, Endocrinology, chemistry, Internal medicine, Meeting Abstract, otorhinolaryngologic diseases, medicine, Pharmacology (medical), Inner ear, sense organs, Auditory function, Guanylate cyclase
Abstract

Background In the inner ear, elevated cyclic guanosine 3’-5’-monophospate (cGMP) levels were shown to have a sheltering role for cochlear hair cells and hearing function [1]. However, the individual roles of the two nitric oxide-sensitive guanylyl cyclase isoforms (NO-GC1 and NO-GC2) as cGMP generators in this protective effect are still unclear. The aim of this study was to investigate how the deletion of either one of the a-subunits of NO-GC (NO-GC1 KO or NO-GC2 KO) [2] or deletion of the b1-subunit of NO-GC (NO-GC KO), leading to global lack of NO-GC expression [3], affects hearing function, vulnerability to noise exposure and recovery from acoustic trauma in mice.

Published
2015
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4. The NO-cGMP pathway participates in vascular adaptation to oxidative stress in Nrf2 KO mice

Author

Christina Panknin, Miriam M. Cortese-Krott, Ralf Erkens, C. Krämer, Lisann Krause, Evanthia Mergia, Malte Kelm, Thomas Krenz, and Mathias Weidenbach

Subjects
Pharmacology, Antioxidant, business.industry, medicine.medical_treatment, Wild type, Cellular redox, medicine.disease, medicine.disease_cause, Bioinformatics, Phenotype, Cell biology, Meeting Abstract, medicine, Pharmacology (medical), Endothelial dysfunction, Adaptation, business, Transcription factor, Oxidative stress
Abstract

Background Endothelial dysfunction is considered both as cause and consequence of oxidative stress. Mice lacking the transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2 KO) can be considered as a model of chronic adaption of the organism to oxidative stress, as they miss a key master switch controlling the expression of antioxidant and protective enzymes involved in the regulation of the cellular redox state. In this study we aimed to investigate the coronary and vascular phenotype and systemic hemodynamics of these mice compared to wild type (WT) littermates.

Published
2015
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5. Functions of NO-GC1 and NO-GC2 in pain processing

Author

Oliver Drees, Andreas Friebe, Achim Schmidtko, Catherine Isabell Real, Jonas Petersen, Evanthia Mergia, Doris Koesling, and Ruirui Lu

Subjects
Pharmacology, Gene isoform, business.industry, Protein subunit, Chronic pain, Nerve injury, Bioinformatics, medicine.disease, Spinal cord, Nitric oxide, chemistry.chemical_compound, Nociception, medicine.anatomical_structure, chemistry, Meeting Abstract, Neuropathic pain, Medicine, Pharmacology (medical), medicine.symptom, business
Abstract

Background Chronic pain in response to tissue inflammation (inflammatory pain) or nerve injury (neuropathic pain) is often unresponsive to currently available treatments. A large body of evidence indicates that production of nitric oxide (NO) and activation of NO-sensitive guanylyl cyclase (NO-GC) essentially contributes to the processing of chronic pain. NO-GC is a heterodimer consisting of one a subunit (a1 or a2) and one b1 subunit and exists in two isoforms (NO-GC1 and NOGC2). However, the functional role of NO-GC1 and NO-GC2 in pain processing remains poorly understood. Here, we investigated the expression of NO-GC isoforms in pain-relevant tissues (dorsal root ganglia and the spinal cord) and characterized the nociceptive behavior of mice lacking a1 or a2 in models of acute nociceptive, inflammatory and neuropathic pain.

Published
2015
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6. NO signalling in synaptic transmission

Author

Angela Neitz, Thomas Mittmann, Evanthia Mergia, and Doris Koesling

Subjects
Pharmacology, Gene isoform, biology, Long-term potentiation, Neurotransmission, biology.organism_classification, Nitric oxide, Cell biology, chemistry.chemical_compound, Signalling, chemistry, Enos, Retrograde signaling, Oral Presentation, Pharmacology (medical), Neurotransmitter
Abstract

Background The NO/cGMP signaling cascade has been proposed to play a role in long-term potentiation (LTP) and the modulation of synaptic transmission. Nitric oxide is formed enzymatically by NO synthases (NOS); two NOS, the endothelial and neuronal isoform (eNOS, nNOS) produce NO as a signalling molecule. Functionally, NO has been reported to act as a retrograde messenger that is generated postsynaptically to increase the neurotransmitter release presynaptically. The NO effects are mediated by the NO-sensitive guanylyl cyclases (NO-GC), which by the formation of cGMP transduce the NO signal. Two functionally indistinguishable isoforms of the NO-GCs, NO-GC1 and NO-GC2 exist.

Published
2011
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7. Functional roles of isoforms of NO-sensitive guanylyl cyclase

Author

Gisela Grecksch, Volker Hoellt, Feras Taqatqeh, Evanthia Mergia, Thomas Mittmann, Doris Koesling, and Axel Becker

Subjects
Pharmacology, Gene isoform, Chemistry, Pharmacology toxicology, GUCY2D, Pharmacology (medical), Guanylate cyclase 2C, Subcellular localization, Cell biology, Guanylate cyclase
Abstract

Two isoforms of NO-sensitive GC have been identified to date that share regulatory properties but differ in the subcellular localization; the more ubiquitously expressed α1β1 heterodimer (α1-GC) and the α2β1 isoform (α2-GC) mainly expressed in brain. Knock-out mice in which either one the α subunits is deleted reveal a loss of the respective GC isoform. The α1-GC and α2-GC KO mice do not show up-regulation of the remaining non-deleted isoform and therefore provide information about the functional roles of the isoforms.

Published
2007
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9. News within NO/cGMP signalling

Author

Andreas Friebe, Doris Koesling, Evanthia Mergia, Michael Russwurm, and Florian Müllershausen

Subjects
Signalling, Chemistry, General Medicine, Cell biology
Published
2003
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