Search

Your search keyword '"Görlach, A. (Agnes)"' showing total 5 results
Start Over Author "Görlach, A. (Agnes)"
5 results on '"Görlach, A. (Agnes)"'

1. Transit of H₂O₂ across the endoplasmic reticulum membrane is not sluggish

Author

Appenzeller-Herzog, C. (Christian), Bánhegyi, G. (Gabor), Bogeski, I. (Ivan), Davies, K. J. (Kelvin J.A.), Delaunay-Moisan, A. (Agnès), Forman, H. J. (Henry Jay), Görlach, A. (Agnes), Kietzmann, T. (Thomas), Laurindo, F. (Francisco), Margittai, E. (Eva), Meyer , A. J. (Andreas J.), Riemer, J. (Jan), Rützler, M. (Michael), Simmen, T. (Thomas), Sitia, R. (Roberto), Toledano, M. B. (Michel B.), and Touw, I. P. (Ivo P.)

Abstract

Cellular metabolism provides various sources of hydrogen peroxide (H₂O₂) in different organelles and compartments. The suitability of H₂O₂ as an intracellular signaling molecule therefore also depends on its ability to pass cellular membranes. The propensity of the membranous boundary of the endoplasmic reticulum (ER) to let pass H₂O₂ has been discussed controversially. In this essay, we challenge the recent proposal that the ER membrane constitutes a simple barrier for H₂O₂ diffusion and support earlier data showing that (i) ample H₂O₂ permeability of the ER membrane is a prerequisite for signal transduction, (ii) aquaporin channels are crucially involved in the facilitation of H₂O₂ permeation, and (iii) a proper experimental framework not prone to artifacts is necessary to further unravel the role of H₂O₂ permeation in signal transduction and organelle biology.

Published
2016

2. Differential transcriptional regulation of hypoxia-inducible factor-1α by arsenite under normoxia and hypoxia:involvement of Nrf2

Author

al Taleb, Z. (Zukaa), Petry, A. (Andreas), Franklin Chi, T. (Tabughang), Mennerich, D. (Daniela), Görlach, A. (Agnes), Dimova, E. Y. (Elitsa Y.), and Kietzmann, T. (Thomas)

Subjects
Arsenite As(III), NADPH enzyme oxidase 4 (NOX4), Reactive oxygen species (ROS), Hypoxia-inducible factor 1 (HIF-1 α ), Mitogen-activated protein kinase (MAPK)
Abstract

Arsenite (As(III)) is widely distributed in nature and can be found in water, food, and air. There is significant evidence that exposure to As(III) is associated with human cancers originated from liver, lung, skin, bladder, kidney, and prostate. Hypoxia plays a role in tumor growth and aggressiveness; adaptation to it is, at least to a large extent, mediated by hypoxia-inducible factor-1α (HIF-1α). In the current study, we investigated As(III) effects on HIF-1α under normoxia and hypoxia in the hepatoma cell line HepG2. We found that As(III) increased HIF-1α protein levels under normoxia while the hypoxia-mediated induction of HIF1α was reduced. Thereby, the As(III) effects on HIF-1α were dependent on both, transcriptional regulation via the transcription factor Nrf2 mediated by NOX4, PI3K/Akt, and ERK1/2 as well as by modulation of HIF-1α protein stability. In line, the different effects of As(III) via participation of HIF-1α and Nrf2 were also seen in tube formation assays with endothelial cells where knockdown of Nrf2 and HIF-1α abolished As(III) effects. Overall, the present study shows that As(III) is a potent inducer of HIF-1α under normoxia but not under hypoxia which may explain, in part, its carcinogenic as well as anti-carcinogenic actions.

Published
2016

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

4. Reactive oxygen species, nutrition, hypoxia and diseases:problems solved?

Author

Görlach, A. (Agnes), Dimova, E. Y. (Elitsa Y. ), Petry, A. (Andreas), Martínez-Ruiz, A. (Antonio), Hernansanz-Agustín, P. (Pablo), Rolo, A. P. (Anabela P.), Palmeira, C. M. (Carlos M.), and Kietzmann, T. (Thomas)

Subjects
Oxygen, Metabolism, Diabetes, Diseases, Free radicals, Obesity, Diets, Hypoxia, Mitochondria
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

5. Mitochondrial dysfunction due to lack of manganese superoxide dismutase promotes hepatocarcinogenesis

Author

Konzack, A. (Anja), Jakupovic, M. (Mirza), Kubaichuk, K. (Kateryna), Görlach, A. (Agnes), Dombrowski, F. (Frank), Miinalainen, I. (Ilkka), Sormunen, R. (Raija), Kietzmann, T. (Thomas), Konzack, A. (Anja), Jakupovic, M. (Mirza), Kubaichuk, K. (Kateryna), Görlach, A. (Agnes), Dombrowski, F. (Frank), Miinalainen, I. (Ilkka), Sormunen, R. (Raija), and Kietzmann, T. (Thomas)

Abstract

Aims: One of the cancer hallmarks is mitochondrial dysfunction associated with oxidative stress. Among the first line of defense against oxidative stress is the dismutation of superoxide radicals, which in the mitochondria is carried out by manganese superoxide dismutase (MnSOD). Accordingly, carcinogenesis would be associated with a dysregulation in MnSOD expression. However, the association studies available so far are conflicting, and no direct proof concerning the role of MnSOD as a tumor promoter or suppressor has been provided. Therefore, we investigated the role of MnSOD in carcinogenesis by studying the effect of MnSOD deficiency in cells and in the livers of mice. Results: We found that loss of MnSOD in hepatoma cells contributed to their conversion toward a more malignant phenotype, affecting all cellular properties generally associated with metabolic transformation and tumorigenesis. In vivo, hepatocyte-specific MnSOD-deficient mice showed changed organ architecture, increased expression of tumor markers, and a faster response to carcinogenesis. Moreover, deficiency of MnSOD in both the in vitro and in vivo model reduced β-catenin and hypoxia-inducible factor-1⍺ levels. Innovation: The present study shows for the first time the important correlation between MnSOD presence and the regulation of two major pathways involved in carcinogenesis, the Wnt/β-catenin and hypoxia signaling pathway. Conclusion: Our study points toward a tumor suppressive role of MnSOD in liver, where the Wnt/β-catenin and hypoxia pathway may be crucial elements.

Published
2015

Catalog

Books, media, physical & digital resources
See catalog results