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43 results on '"Petry, Andreas"'

1. MondoA drives malignancy in B-ALL through enhanced adaptation to metabolic stress

Author

Sipol, Alexandra, Hameister, Erik, Xue, Busheng, Hofstetter, Julia, Barenboim, Maxim, Öllinger, Rupert, Jain, Gaurav, Prexler, Carolin, Rubio, Rebeca Alba, Baldauf, Michaela C., Franchina, Davide G., Petry, Andreas, Schmäh, Juliane, Thiel, Uwe, Görlach, Agnes, Cario, Gunnar, Brenner, Dirk, Richter, Günther H.S., Grünewald, Thomas G.P., Rad, Roland, Wolf, Elmar, Ruland, Jürgen, Sorensen, Poul H., and Burdach, Stefan E.G.

Published
2022
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2. Inflammation and Fibrosis in Progeria: Organ-Specific Responses in an HGPS Mouse Model.

Author

Krüger, Peter, Schroll, Moritz, Fenzl, Felix, Lederer, Eva-Maria, Hartinger, Ramona, Arnold, Rouven, Cagla Togan, Deniz, Guo, Runjia, Liu, Shiyu, Petry, Andreas, Görlach, Agnes, and Djabali, Karima

Subjects
POISONS, PROGERIN, CARDIOVASCULAR system, GENETIC disorders, TISSUE remodeling, LUNGS
Abstract

Hutchinson–Gilford Progeria Syndrome (HGPS) is an extremely rare genetic disorder that causes accelerated aging, due to a pathogenic variant in the LMNA gene. This pathogenic results in the production of progerin, a defective protein that disrupts the nuclear lamina's structure. In our study, we conducted a histopathological analysis of various organs in the LmnaG609G/G609G mouse model, which is commonly used to study HGPS. The objective of this study was to show that progerin accumulation drives systemic but organ-specific tissue damage and accelerated aging phenotypes. Our findings show significant fibrosis, inflammation, and dysfunction in multiple organ systems, including the skin, cardiovascular system, muscles, lungs, liver, kidneys, spleen, thymus, and heart. Specifically, we observed severe vascular fibrosis, reduced muscle regeneration, lung tissue remodeling, depletion of fat in the liver, and disruptions in immune structures. These results underscore the systemic nature of the disease and suggest that chronic inflammation and fibrosis play crucial roles in the accelerated aging seen in HGPS. Additionally, our study highlights that each organ responds differently to the toxic effects of progerin, indicating that there are distinct mechanisms of tissue-specific damage. [ABSTRACT FROM AUTHOR]

Published
2024
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10. MondoA Drives Malignancy in cALL through Enhanced Adaptation to Metabolic Stress

Author

Sipol, Alexandra, primary, Hameister, Erik, additional, Xue, Busheng, additional, Petry, Andreas, additional, Prexler, Carolin, additional, Barenboim, Maxim, additional, Rubio, Rebeca Alba, additional, Baldauf, Michaela C., additional, Franchina, Davide G., additional, Schmaeh, Juliane, additional, Richter, Guenther, additional, Cario, Gunnar, additional, Grünewald, Thomas G.P., additional, Görlach, Agnes, additional, Brenner, Dirk, additional, Ruland, Jürgen, additional, Sorensen, Poul H., additional, and Burdach, Stefan E.G., additional

Published
2020
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18. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul, Bernlohr, David, Ruskovska, Tatjana, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., Di Lisa, Fabio, and Daiber, Andreas

Subjects
Basic medicine
Abstract

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

Published
2017

19. The epigenetic landscape related to reactive oxygen species formation in the cardiovascular system

Author

Kietzmann, Thomas, Petry, Andreas, Shvetsova, Antonina, Gerhold, Joachim M, and Görlach, Agnes

Subjects
Cardiovascular Diseases, Animals, Humans, Reactive Oxygen Species, Themed Section: Review Articles, Cardiovascular System, Epigenesis, Genetic
Abstract

Cardiovascular diseases are among the leading causes of death worldwide. Reactive oxygen species (ROS) can act as damaging molecules but also represent central hubs in cellular signalling networks. Increasing evidence indicates that ROS play an important role in the pathogenesis of cardiovascular diseases, although the underlying mechanisms and consequences of pathophysiologically elevated ROS in the cardiovascular system are still not completely resolved. More recently, alterations of the epigenetic landscape, which can affect DNA methylation, post-translational histone modifications, ATP-dependent alterations to chromatin and non-coding RNA transcripts, have been considered to be of increasing importance in the pathogenesis of cardiovascular diseases. While it has long been accepted that epigenetic changes are imprinted during development or even inherited and are not changed after reaching the lineage-specific expression profile, it becomes more and more clear that epigenetic modifications are highly dynamic. Thus, they might provide an important link between the actions of ROS and cardiovascular diseases. This review will provide an overview of the role of ROS in modulating the epigenetic landscape in the context of the cardiovascular system.This article is part of a themed section on Redox Biology and Oxidative Stress in Health and Disease. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.12/issuetoc.

Published
2017

20. European contribution to the study of ROS:a summary of the findings and prospects for the future from the COST Action BM1203 (EU-ROS)

Author

Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Stella, Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, João G., Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec–butuner, Bilge, Dias, Irundika, Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S., Fladmark, Kari E., Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jinjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, Mcbean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Milos, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T.N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-mañas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalçın, A. Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., di Lisa, Fabio, Daiber, Andreas, Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Stella, Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, João G., Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec–butuner, Bilge, Dias, Irundika, Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S., Fladmark, Kari E., Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jinjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, Mcbean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Milos, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T.N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-mañas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalçın, A. Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H.H.W., di Lisa, Fabio, and Daiber, Andreas

Abstract

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

Published
2017

21. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

MS Nefrologie, Regenerative Medicine and Stem Cells, Circulatory Health, Nefro Vasculaire Geneeskunde, Other research (not in main researchprogram), Egea, Javier, Fabregat, Isabel, Frapart, Yves M, Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G, Lopez, Manuela G, Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul J, Abbas, Kahina, Ademowo, Opeyemi S, Afonso, Catarina B, Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M, Barbosa, Rui M, Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P, Brito, Paula M, Carrara, Guia, Casas, Ana I, Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S, Costa, João G, Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec-Butuner, Bilge, Dias, Irundika H K, Dunn, Joe Dan, Edson, Amanda J, El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S, Fladmark, Kari E, Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen L, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A, Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J, Meredith, Stuart P, Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Miloš, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T N, Oelze, Matthias, Oliveira, Nuno G, Palmeira, Carlos M, Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G, Pitt, Andrew R, Poulsen, Henrik E, Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-Mañas, Leocadio, Rolo, Anabela P, Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L, Soldati, Thierry, Sousa, Bebiana C, Spickett, Corinne M, Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A, Yalçın, A Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M, Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H H W, Di Lisa, Fabio, Daiber, Andreas, MS Nefrologie, Regenerative Medicine and Stem Cells, Circulatory Health, Nefro Vasculaire Geneeskunde, Other research (not in main researchprogram), Egea, Javier, Fabregat, Isabel, Frapart, Yves M, Ghezzi, Pietro, Görlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G, Lopez, Manuela G, Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vina, Jose, Winyard, Paul J, Abbas, Kahina, Ademowo, Opeyemi S, Afonso, Catarina B, Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M, Barbosa, Rui M, Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertrán, Esther, Bindoli, Alberto, Bottari, Serge P, Brito, Paula M, Carrara, Guia, Casas, Ana I, Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S, Costa, João G, Cuadrado, Antonio, My-Chan Dang, Pham, De Smet, Barbara, Debelec-Butuner, Bilge, Dias, Irundika H K, Dunn, Joe Dan, Edson, Amanda J, El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Péter, Fernandes, Ana S, Fladmark, Kari E, Förstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltán, Görbe, Anikó, Griffiths, Helen L, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustín, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Dürr, Pidder, Jaquet, Vincent, Joles, Jaap A, Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Korkmaz, Kemal Sami, Koziel, Rafal, Kračun, Damir, Krause, Karl-Heinz, Křen, Vladimír, Krieg, Thomas, Laranjinha, João, Lazou, Antigone, Li, Huige, Martínez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J, Meredith, Stuart P, Messens, Joris, Miguel, Verónica, Mikhed, Yuliya, Milisav, Irina, Milković, Lidija, Miranda-Vizuete, Antonio, Mojović, Miloš, Monsalve, María, Mouthuy, Pierre-Alexis, Mulvey, John, Münzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T N, Oelze, Matthias, Oliveira, Nuno G, Palmeira, Carlos M, Papaevgeniou, Nikoletta, Pavićević, Aleksandra, Pedre, Brandán, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G, Pitt, Andrew R, Poulsen, Henrik E, Prieto, Ignacio, Rigobello, Maria Pia, Robledinos-Antón, Natalia, Rodríguez-Mañas, Leocadio, Rolo, Anabela P, Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schröder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L, Soldati, Thierry, Sousa, Bebiana C, Spickett, Corinne M, Stancic, Ana, Stasia, Marie José, Steinbrenner, Holger, Stepanić, Višnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentová, Kateřina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A, Yalçın, A Suha, Yelisyeyeva, Olha, Žarković, Neven, Zatloukalová, Martina, Zielonka, Jacek, Touyz, Rhian M, Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H H W, Di Lisa, Fabio, and Daiber, Andreas

Published
2017

23. Immunoproteasome subunit ß5i/LMP7-deficiency in atherosclerosis

Author

Hewing, Bernd, primary, Ludwig, Antje, additional, Dan, Cristian, additional, Pötzsch, Max, additional, Hannemann, Carmen, additional, Petry, Andreas, additional, Lauer, Dilyara, additional, Görlach, Agnes, additional, Kaschina, Elena, additional, Müller, Dominik N., additional, Baumann, Gert, additional, Stangl, Verena, additional, Stangl, Karl, additional, and Wilck, Nicola, additional

Published
2017
Full Text
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24. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

Egea, Javier, primary, Fabregat, Isabel, additional, Frapart, Yves M., additional, Ghezzi, Pietro, additional, Görlach, Agnes, additional, Kietzmann, Thomas, additional, Kubaichuk, Kateryna, additional, Knaus, Ulla G., additional, Lopez, Manuela G., additional, Olaso-Gonzalez, Gloria, additional, Petry, Andreas, additional, Schulz, Rainer, additional, Vina, Jose, additional, Winyard, Paul, additional, Abbas, Kahina, additional, Ademowo, Opeyemi S., additional, Afonso, Catarina B., additional, Andreadou, Ioanna, additional, Antelmann, Haike, additional, Antunes, Fernando, additional, Aslan, Mutay, additional, Bachschmid, Markus M., additional, Barbosa, Rui M., additional, Belousov, Vsevolod, additional, Berndt, Carsten, additional, Bernlohr, David, additional, Bertrán, Esther, additional, Bindoli, Alberto, additional, Bottari, Serge P., additional, Brito, Paula M., additional, Carrara, Guia, additional, Casas, Ana I., additional, Chatzi, Afroditi, additional, Chondrogianni, Niki, additional, Conrad, Marcus, additional, Cooke, Marcus S., additional, Costa, João G., additional, Cuadrado, Antonio, additional, My-Chan Dang, Pham, additional, De Smet, Barbara, additional, Debelec–Butuner, Bilge, additional, Dias, Irundika H.K., additional, Dunn, Joe Dan, additional, Edson, Amanda J., additional, El Assar, Mariam, additional, El-Benna, Jamel, additional, Ferdinandy, Péter, additional, Fernandes, Ana S., additional, Fladmark, Kari E., additional, Förstermann, Ulrich, additional, Giniatullin, Rashid, additional, Giricz, Zoltán, additional, Görbe, Anikó, additional, Griffiths, Helen, additional, Hampl, Vaclav, additional, Hanf, Alina, additional, Herget, Jan, additional, Hernansanz-Agustín, Pablo, additional, Hillion, Melanie, additional, Huang, Jingjing, additional, Ilikay, Serap, additional, Jansen-Dürr, Pidder, additional, Jaquet, Vincent, additional, Joles, Jaap A., additional, Kalyanaraman, Balaraman, additional, Kaminskyy, Danylo, additional, Karbaschi, Mahsa, additional, Kleanthous, Marina, additional, Klotz, Lars-Oliver, additional, Korac, Bato, additional, Korkmaz, Kemal Sami, additional, Koziel, Rafal, additional, Kračun, Damir, additional, Krause, Karl-Heinz, additional, Křen, Vladimír, additional, Krieg, Thomas, additional, Laranjinha, João, additional, Lazou, Antigone, additional, Li, Huige, additional, Martínez-Ruiz, Antonio, additional, Matsui, Reiko, additional, McBean, Gethin J., additional, Meredith, Stuart P., additional, Messens, Joris, additional, Miguel, Verónica, additional, Mikhed, Yuliya, additional, Milisav, Irina, additional, Milković, Lidija, additional, Miranda-Vizuete, Antonio, additional, Mojović, Miloš, additional, Monsalve, María, additional, Mouthuy, Pierre-Alexis, additional, Mulvey, John, additional, Münzel, Thomas, additional, Muzykantov, Vladimir, additional, Nguyen, Isabel T.N., additional, Oelze, Matthias, additional, Oliveira, Nuno G., additional, Palmeira, Carlos M., additional, Papaevgeniou, Nikoletta, additional, Pavićević, Aleksandra, additional, Pedre, Brandán, additional, Peyrot, Fabienne, additional, Phylactides, Marios, additional, Pircalabioru, Gratiela G., additional, Pitt, Andrew R., additional, Poulsen, Henrik E., additional, Prieto, Ignacio, additional, Rigobello, Maria Pia, additional, Robledinos-Antón, Natalia, additional, Rodríguez-Mañas, Leocadio, additional, Rolo, Anabela P., additional, Rousset, Francis, additional, Ruskovska, Tatjana, additional, Saraiva, Nuno, additional, Sasson, Shlomo, additional, Schröder, Katrin, additional, Semen, Khrystyna, additional, Seredenina, Tamara, additional, Shakirzyanova, Anastasia, additional, Smith, Geoffrey L., additional, Soldati, Thierry, additional, Sousa, Bebiana C., additional, Spickett, Corinne M., additional, Stancic, Ana, additional, Stasia, Marie José, additional, Steinbrenner, Holger, additional, Stepanić, Višnja, additional, Steven, Sebastian, additional, Tokatlidis, Kostas, additional, Tuncay, Erkan, additional, Turan, Belma, additional, Ursini, Fulvio, additional, Vacek, Jan, additional, Vajnerova, Olga, additional, Valentová, Kateřina, additional, Van Breusegem, Frank, additional, Varisli, Lokman, additional, Veal, Elizabeth A., additional, Yalçın, A. Suha, additional, Yelisyeyeva, Olha, additional, Žarković, Neven, additional, Zatloukalová, Martina, additional, Zielonka, Jacek, additional, Touyz, Rhian M., additional, Papapetropoulos, Andreas, additional, Grune, Tilman, additional, Lamas, Santiago, additional, Schmidt, Harald H.H.W., additional, Di Lisa, Fabio, additional, and Daiber, Andreas, additional

Published
2017
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26. Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved?

Author

Görlach, Agnes, Dimova, Elitsa Y, Petry, Andreas, Martínez-Ruiz, Antonio, Hernansanz-Agustín, Pablo, Rolo, Anabela P, Palmeira, Carlos M, and Kietzmann, Thomas

Subjects
Nucleocytoplasmic Transport Proteins, Diabetes, NF-kappa B, Nutritional Requirements, Diseases, Free radicals, Diets, Pregnancy Proteins, Atherosclerosis, Mitochondria, Oxygen, Oxidative Stress, Metabolism, Diabetes Mellitus, Type 2, Gene Expression Regulation, Neoplasms, Animals, Humans, Obesity, Mitogen-Activated Protein Kinases, Hypoxia, Energy Metabolism, Reactive Oxygen Species, Signal Transduction
Abstract

Within the last twenty years the view on reactive oxygen species (ROS) has changed; they are no longer only considered to be harmful but also necessary for cellular communication and homeostasis in different organisms ranging from bacteria to mammals. In the latter, ROS were shown to modulate diverse physiological processes including the regulation of growth factor signaling, the hypoxic response, inflammation and the immune response. During the last 60-100 years the life style, at least in the Western world, has changed enormously. This became obvious with an increase in caloric intake, decreased energy expenditure as well as the appearance of alcoholism and smoking; These changes were shown to contribute to generation of ROS which are, at least in part, associated with the occurrence of several chronic diseases like adiposity, atherosclerosis, type II diabetes, and cancer. In this review we discuss aspects and problems on the role of intracellular ROS formation and nutrition with the link to diseases and their problematic therapeutical issues.

Published
2015

28. Characterization of novel NADPH oxidases in endothelial cells under basal and stress conditions

Author

Petry, Andreas

Subjects
urogenital system, FOS: Chemical sciences, NADPH oxidases, cardiovascular system, circulatory and respiratory physiology
Abstract

Increased levels of reactive oxygen species (ROS) contribute to vascular diseases like pulmonary hypertension and atherosclerosis. Although a NOX2-containing NADPH oxidase similar to the neutrophil one has been described to be active in endothelial cells, the contribution of newly discovered NOX homologues (NOX1-NOX5) was still unclear. Therefore, the overall aim of this study was to better characterize the expression, regulation and function of NOX homologues in different endothelial cell models. First, we could demonstrate the presence of NOX1, NOX2, NOX4, NOX5 including NOX5S as well as p22phox mRNA and protein levels in Ea.Hy926 or HMEC-1 cells. Furthermore, NOX5 protein was also present in endothelial and smooth muscle cells in the vascular wall of spleen and lung tissue. We found that NOX2, NOX4 and NOX5 were present in an intracellular perinuclear compartment, whereby NOX2 and NOX4 could be localized simultaneously in one cell. NOX2, NOX4, NOX5 were able to interact with p22phox and overexpression of NOX2, NOX4 and NOX5 increased ROS generation, although NOX5-dependent ROS generation did not require the presence of p22phox. NOX2, NOX4 and NOX5 also increased endothelial proliferation while depletion of NOX2, NOX4 and NOX5 decreased ROS generation, proliferation and tube forming ability indicating angiogenic activity under basal conditions. NOX2- and NOX4-induced proliferation was mediated by p38 MAP kinase. Although NOX1 expression as well as the expression of its regulatory subunits NOXO1 and NOXA1 was detectable in endothelial cells, depletion of NOX1 did not significantly affect basal ROS generation or proliferation of endothelial cells. Second, we could demonstrate the upregulation of NOX2, NOX5 and NOX5S after thrombin stimulation in endothelial cells and the modulation of p22phox expression in an ATF4- and XBP1-dependent manner under ER-stress conditions. Cellular stress either by thrombin or UPR also induced ROS generation of endothelial cells. In addition, thrombin induced proliferation and enhanced the tube forming ability of endothelial cells. Thrombin-induced ROS generation, proliferation and tube forming ability were diminished by silencing NOX2 or NOX5, whereas UPR induced ROS generation was inhibited by silencing p22phox as well as by silencing ATF4 or XBP1. In summary, this work provides evidence that in endothelial cells, NOX2, NOX4 and NOX5, but not NOX1, contribute to basal ROS generation, proliferation and angiogenesis and that the NOX proteins NOX2 and NOX5 as well as p22phox play an important role in the response to thrombin and ER-stress providing new insights in endothelial function and redox signaling.

Published
2009
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40. The HIF1 target gene NOX2 promotes angiogenesis through urotensin-II.

Author

Diebold, Isabel, Petry, Andreas, Sabrane, Karim, Djordjevic, Talija, Hess, John, and rlach, Agnes Gö

Subjects
*NEOVASCULARIZATION, *UROTENSINS, *VASOACTIVE intestinal peptide, *VASCULAR endothelial growth factors, *BLOOD vessels
Abstract

Urotensin-II (U-II) has been considered as one of the most potent vasoactive peptides, although its physiological and pathophysiological role is still not finally resolved. Recent evidence suggests that it promotes angiogenic responses in endothelial cells, although the underlying signalling mechanisms are unclear. Reactive oxygen species derived from NADPH oxidases are major signalling molecules in the vasculature. Because NOX2 is functional in endothelial cells, we investigated the role of the NOX2-containing NADPH oxidase in U-II-induced angiogenesis and elucidated a possible contribution of hypoxia-inducible factor-1 (HIF-1), the master regulator of hypoxic angiogenesis, in the response to U-II. We found that U-II increases angiogenesis in vitro and in vivo, and these responses were prevented by antioxidants, NOX2 knockdown and in Nox2-/- mice. In addition, U-II-induced angiogenesis was dependent on HIF-1. Interestingly, U-II increased NOX2 transcription involving HIF-1, and chromatin immunoprecipitation confirmed NOX2 as a target gene of HIF-1. In support, NOX2 levels were greatly diminished in U-II-stimulated isolated vessels derived from mice deficient in endothelial HIF-1. Conversely, reactive oxygen species derived from NOX2 were required for U-II activation of HIF and upregulation of HIF-1. In line with this, U-II-induced upregulation of HIF-1 was absent in Nox2-/- vessels. Collectively, these findings identified HIF-1 and NOX2 as partners acting in concert to promote angiogenesis in response to U-II. Because U-II has been found to be elevated in cardiovascular disorders and in tumour tissues, this feed-forward mechanism could be an interesting anti-angiogenic therapeutic option in these disorders. [ABSTRACT FROM AUTHOR]

Published
2012
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42. Volumetric optoacoustic tomography enables non-invasive in vivo characterization of impaired heart function in hypoxic conditions

Author

Ivankovic, Ivana, Deán-Ben, Xosé Luís, Lin, Hsiao-Chun A., Zhang, Zuwen, Trautz, Benjamin, Petry, Andreas, Görlach, Agnes, and Razansky, Daniel

Subjects
3. Good health
Abstract

Exposure to chronic hypoxia results in pulmonary hypertension characterized by increased vascular resistance and pulmonary vascular remodeling, changes in functional parameters of the pulmonary vasculature, and right ventricular hypertrophy, which can eventually lead to right heart failure. The underlying mechanisms of hypoxia-induced pulmonary hypertension have still not been fully elucidated while no curative treatment is currently available. Commonly employed pre-clinical analytic methods are largely limited to invasive studies interfering with cardiac tissue or otherwise ex vivo functional studies and histopathology. In this work, we suggest volumetric optoacoustic tomography (VOT) for non-invasive assessment of heart function in response to chronic hypoxia. Mice exposed for 3 consecutive weeks to normoxia or chronic hypoxia were imaged in vivo with heart perfusion tracked by VOT using indocyanide green contrast agent at high temporal (100 Hz) and spatial (200 µm) resolutions in 3D. Unequivocal difference in the pulmonary transit time was revealed between the hypoxic and normoxic conditions concomitant with the presence of pulmonary vascular remodeling within hypoxic models. Furthermore, a beat-to-beat analysis of the volumetric image data enabled identifying and characterizing arrhythmic events in mice exposed to chronic hypoxia. The newly introduced non-invasive methodology for analysis of impaired pulmonary vasculature and heart function under chronic hypoxic exposure provides important inputs into development of early diagnosis and treatment strategies in pulmonary hypertension., Scientific Reports, 9 (1), ISSN:2045-2322

43. European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

Author

YALÇIN, AHMET SUHA, Egea, Javier, Fabregat, Isabel, Frapart, Yves M., Ghezzi, Pietro, Gorlach, Agnes, Kietzmann, Thomas, Kubaichuk, Kateryna, Knaus, Ulla G., Lopez, Manuela G., Olaso-Gonzalez, Gloria, Petry, Andreas, Schulz, Rainer, Vinal, Jose, Winyard, Paul, Abbas, Kahina, Ademowo, Opeyemi S., Afonso, Catarina B., Andreadou, Ioanna, Antelmann, Haike, Antunes, Fernando, Aslan, Mutay, Bachschmid, Markus M., Barbosa, Rui M., Belousov, Vsevolod, Berndt, Carsten, Bernlohr, David, Bertran, Esther, Bindoli, Alberto, Bottari, Serge P., Brito, Paula M., Carrara, Guia, Casas, Ana I., Chatzi, Afroditi, Chondrogianni, Niki, Conrad, Marcus, Cooke, Marcus S., Costa, Joao G., Cuadrado, Antonio, Dang, Pham My-Chan, De Smet, Barbara, Butuner, Bilge Debelec, Dias, Irundika H. K., Dunn, Joe Dan, Edson, Amanda J., El Assar, Mariam, El-Benna, Jamel, Ferdinandy, Peter, Fernandes, Ana S., Fladmark, Kari E., Forstermann, Ulrich, Giniatullin, Rashid, Giricz, Zoltan, Gorbe, Aniko, Griffiths, Helen, Hampl, Vaclav, Hanf, Alina, Herget, Jan, Hernansanz-Agustin, Pablo, Hillion, Melanie, Huang, Jingjing, Ilikay, Serap, Jansen-Durr, Pidder, Jaquet, Vincent, Joles, Jaap A., Kalyanaraman, Balaraman, Kaminskyy, Danylo, Karbaschi, Mahsa, Kleanthous, Marina, Klotz, Lars-Oliver, Korac, Bato, Sami Korkmaz, Kemal, Koziel, Rafal, Kracun, Damir, Krause, Karl-Heinz, Kren, Vladimir, Krieg, Thomas, Laranjinha, Joao, Lazou, Antigone, Li, Huige, Martinez-Ruiz, Antonio, Matsui, Reiko, McBean, Gethin J., Meredith, Stuart P., Messens, Joris, Miguel, Veronica, Mikhed, Yuliya, Milisav, Irina, Milkovic, Lidija, Miranda-Vizuete, Antonio, Mojovic, Milos, Monsalve, Maria, Mouthuy, Pierre-Alexis, Mulvey, John, Munzel, Thomas, Muzykantov, Vladimir, Nguyen, Isabel T. N., Oelze, Matthias, Oliveira, Nuno G., Palmeira, Carlos M., Papaevgeniou, Nikoletta, Pavicevic, Aleksandra, Pedre, Brandan, Peyrot, Fabienne, Phylactides, Marios, Pircalabioru, Gratiela G., Pitt, Andrew R., Poulsen, Henrik E., Prieto, Ignacio, Pia Rigobello, Maria, Robledinos-Anton, Natalia, Rodriguez-Manas, Leocadio, Rolo, Anabela P., Rousset, Francis, Ruskovska, Tatjana, Saraiva, Nuno, Sasson, Shlomo, Schroeder, Katrin, Semen, Khrystyna, Seredenina, Tamara, Shakirzyanova, Anastasia, Smith, Geoffrey L., Soldati, Thierry, Sousa, Bebiana C., Spickett, Corinne M., Stancic, Ana, Stasia, Marie Jose, Steinbrenner, Holger, Stepanic, Visnja, Steven, Sebastian, Tokatlidis, Kostas, Tuncay, Erkan, Turan, Belma, Ursini, Fulvio, Vacek, Jan, Vajnerova, Olga, Valentova, Katerina, Van Breusegem, Frank, Varisli, Lokman, Veal, Elizabeth A., Yalcin, A. Suha, Yelisyeyeva, Olha, Zarkovic, Neven, Zatloukalova, Martina, Zielonka, Jacek, Touyz, Rhian M., Papapetropoulos, Andreas, Grune, Tilman, Lamas, Santiago, Schmidt, Harald H. H. W., Di Lisa, Fabio, and Daiber, Andreas

Subjects
Redox therapeutics, PULMONARY ARTERIAL-HYPERTENSION, Redox signaling, GROWTH-FACTOR-BETA, Reactive nitrogen species, MICROCYSTIN-INDUCED APOPTOSIS, Antioxidants, MANGANESE SUPEROXIDE-DISMUTASE, CHRONIC GRANULOMATOUS-DISEASE, ENDOPLASMIC-RETICULUM STRESS, Oxidative stress, ENDOTHELIAL-CELL MIGRATION, ADENINE-DINUCLEOTIDE PHOSPHATE, NITRIC-OXIDE SYNTHASE, Reactive oxygen species, MITOCHONDRIAL OXIDATIVE STRESS
Abstract

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics briefly described below. The formation of reactive oxygen and nitrogen species (RONS) is an established hallmark of our aerobic environment and metabolism but RONS also act as messengers via redox regulation of essential cellular processes. The fact that many diseases have been found to be associated with oxidative stress established the theory of oxidative stress as a trigger of diseases that can be corrected by antioxidant therapy. However, while experimental studies support this thesis, clinical studies still generate controversial results, due to complex pathophysiology of oxidative stress in humans. For future improvement of antioxidant therapy and better understanding of redox-associated disease progression detailed knowledge on the sources and targets of RONS formation and discrimination of their detrimental or beneficial roles is required. In order to advance this important area of biology and medicine, highly synergistic approaches combining a variety of diverse and contrasting disciplines are needed.

Published
2017

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