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154. Mutations of the TGF-β Type II Receptor BMPR2 in Pulmonary Arterial Hypertension

Author

Machado, Rajiv D., Aldred, Micheala A., James, Victoria, Harrison, Rachel E., Patel, Bhakti, Schwalbe, Edward C., Gruenig, Ekkehard, Janssen, Bart, Koehler, Rolf, Seeger, Werner, Eickelberg, Oliver, Olschewski, Horst, Elliott, Gregory C., Glissmeyer, Eric, Carlquist, John, Kim, Miryoung, Torbicki, Adam, Fijalkowska, Anna, Szewczyk, Grzegorz, Parma, Jasmine, Abramowicz, Marc J., Galie, Nazzareno, Morisaki, Hiroko, Kyotani, Shingo, Nakanishi, Norifumi, Morisaki, Takayuki, Humbert, Marc, Simonneau, Gerald, Sitbon, Olivier, Soubrier, Florent, Coulet, Florence, Morrell, Nicholas W., and Trembath, Richard C.

Published
2006
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164. Identification of genetic elements in metabolism by high-throughput mouse phenotyping

Author

Rozman, Jan, Rathkolb, Birgit, Meehan, Terrence F, Codner, Gemma F, Fiegel, Tanja, Ring, Natalie, Westerberg, Henrik, Greenaway, Simon, Sneddon, Duncan, Morgan, Hugh, Loeffler, Jorik, Stewart, Michelle E, Ramirez-Solis, Ramiro, Mason, Jeremy, Bradley, Allan, Skarnes, William C, Steel, Karen P, Maguire, Simon A, Dench, Joshua, Lafont, David, Vancollie, Valerie E, Pearson, Selina A, Gates, Amy S, Sanderson, Mark, Haselimashhadi, Hamed, Shannon, Carl, Anthony, Lauren F E, Sumowski, Maksymilian T, McLaren, Robbie S B, Doe, Brendan, Wardle-Jones, Hannah, Griffiths, Mark N D, Galli, Antonella, Swiatkowska, Agnieszka, Isherwood, Christopher M, Consortium, IMPC, Speak, Anneliese O, Cambridge, Emma L, Wilson, Heather M, Caetano, Susana S, Maguire, Anna Karin B, Adams, David J, Bottomley, Joanna, Ryder, Ed, Gleeson, Diane, Pouilly, Laurent, Hough, Tertius, Rousseau, Stephane, Auburtin, Aurélie, Reilly, Patrick, Ayadi, Abdel, Selloum, Mohammed, Wood, Joshua A, Clary, Dave, Havel, Peter, Tolentino, Todd, Tolentino, Heather, Mallon, Ann-Marie, Schuchbauer, Mike, Pedroia, Sheryl, Trainor, Amanda, Djan, Esi, Pham, Milton, Huynh, Alison, De Vera, Vincent, Seavitt, John, Gallegos, Juan, Garza, Arturo, Wells, Sara, Mangin, Elise, Senderstrom, Joel, Lazo, Iride, Mowrey, Kate, Bohat, Ritu, Samaco, Rodney, Veeraragavan, Surabi, Beeton, Christine, Kalaga, Sowmya, Kelsey, Lois, Santos, Luis, Vukobradovic, Igor, Berberovic, Zorana, Owen, Celeste, Qu, Dawei, Guo, Ruolin, Newbigging, Susan, Morikawa, Lily, Law, Napoleon, Shang, Xueyuan, Feugas, Patricia, Lelliott, Christopher J, Wang, Yanchun, Eskandarian, Mohammad, Zhu, Yingchun, Penton, Patricia, Laurin, Valerie, Clarke, Shannon, Lan, Qing, Sleep, Gillian, Creighton, Amie, Jacob, Elsa, White, Jacqueline K, Danisment, Ozge, Gertsenstein, Marina, Pereira, Monica, MacMaster, Suzanne, Tondat, Sandra, Carroll, Tracy, Cabezas, Jorge, Hunter, Jane, Clark, Greg, Bubshait, Mohammed, Oestereicher, Manuela A, Sorg, Tania, Miller, David, Sohel, Khondoker, Adissu, Hibret, Ganguly, Milan, Bezginov, Alexandr, Chiani, Francesco, Di Pietro, Chiara, Di Segni, Gianfranco, Ermakova, Olga, Ferrara, Filomena, Champy, Marie-France, Fruscoloni, Paolo, Gambadoro, Aalessia, Gastaldi, Serena, Golini, Elisabetta, La Sala, Gina, Mandillo, Silvia, Marazziti, Daniela, Massimi, Marzia, Matteoni, Rafaele, Orsini, Tiziana, Bower, Lynette R, Pasquini, Miriam, Raspa, Marcello, Rauch, Aline, Rossi, Gianfranco, Rossi, Nicoletta, Putti, Sabrina, Scavizzi, Ferdinando, Tocchini-Valentini, Giuseppe D, Wakana, Shigeharu, Suzuki, Tomohiro, Reynolds, Corey L, Tamura, Masaru, Kaneda, Hideki, Furuse, Tamio, Kobayashi, Kimio, Miura, Ikuo, Yamada, Ikuko, Obata, Yuichi, Yoshiki, Atsushi, Ayabe, Shinya, Chambers, J Nicole, Flenniken, Ann M, Chalupsky, Karel, Seisenberger, Claudia, Bürger, Antje, Beig, Joachim, Kühn, Ralf, Hörlein, Andreas, Schick, Joel, Oritz, Oskar, Giesert, Florian, Graw, Jochen, Murray, Stephen A, Ollert, Markus, Schmidt-Weber, Carsten, Stoeger, Tobias, Önder Yildirim, Ali, Eickelberg, Oliver, Klopstock, Thomas, Busch, Dirk H, Bekeredjian, Raffi, Zimmer, Andreas, Jacobsen, Jules O, Nutter, Lauryl M J, Smedley, Damian, Dickinson, Mary E, Benso, Frank, Morse, Iva, Kim, Hyoung-Chin, Lee, Ho, Cho, Soo Young, Svenson, Karen L, West, David, Tocchini-Valentini, Glauco P, Schütt, Christine, Beaudet, Arthur L, Bosch, Fatima, Braun, Robert B, Dobbie, Michael S, Gao, Xiang, Herault, Yann, Moshiri, Ala, Moore, Bret A, Kent Lloyd, K. C., McKerlie, Colin, Ravindranath, Aakash Chavan, Masuya, Hiroshi, Tanaka, Nobuhiko, Flicek, Paul, Parkinson, Helen E, Sedlacek, Radislav, Seong, Je Kyung, Wang, Chi-Kuang Leo, Moore, Mark, Brown, Steve D, Tschöp, Matthias H, Leuchtenberger, Stefanie, Wurst, Wolfgang, Klingenspor, Martin, Wolf, Eckhard, Beckers, Johannes, Machicao, Fausto, Peter, Andreas, Staiger, Harald, Häring, Hans-Ulrich, Grallert, Harald, Campillos, Monica, Sharma, Sapna, Maier, Holger, Fuchs, Helmut, Gailus-Durner, Valerie, Werner, Thomas, Hrabe de Angelis, Martin, Aguilar-Pimentel, Antonio, Becker, Lore, Treise, Irina, Moreth, Kristin, Garrett, Lillian, Kistler, Martin, Hölter, Sabine M, Zimprich, Annemarie, Marschall, Susan, Amarie, Oana V, Calzada-Wack, Julia, Neff, Frauke, Brachthäuser, Laura, Lengger, Christoph, Stoeger, Claudia, Zapf, Lilly, Willershäuser, Monja, Cho, Yi-Li, da Silva-Buttkus, Patricia, Kraiger, Markus J, Mayer-Kuckuk, Philipp, Gampe, Karen Kristine, Wu, Moya, Conte, Nathalie, Warren, Jonathan, Chen, Chao-Kung, Tudose, Ilinca, Brommage, Robert, Relac, Mike, Matthews, Peter, Cater, Heather L, Natukunda, Helen P, Cleak, James, Teboul, Lydia M, Clementson-Mobbs, Sharon, Szoke-Kovacs, Zsombor, Walling, Alison P, Johnson, Sara J, Rozman, Jan [0000-0002-8035-8904], Kistler, Martin [0000-0003-0116-7761], Mason, Jeremy [0000-0002-2796-5123], Lelliott, Christopher J [0000-0001-8087-4530], Herault, Yann [0000-0001-7049-6900], Kent Lloyd, KC [0000-0002-5318-4144], McKerlie, Colin [0000-0002-2232-0967], Flicek, Paul [0000-0002-3897-7955], Maier, Holger [0000-0003-2514-8290], Fuchs, Helmut [0000-0002-5143-2677], Hrabe de Angelis, Martin [0000-0002-7898-2353], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, Blood Glucose, Candidate gene, Cancer Research, Basal Metabolism/genetics, Gene regulatory network, Obesity/genetics, genetics [Metabolic Diseases], General Physics and Astronomy, Genome-wide association study, Genome, Mice, genetics [Obesity], Triglycerides/metabolism, 2.1 Biological and endogenous factors, Gene Regulatory Networks, Aetiology, lcsh:Science, metabolism [Blood Glucose], Mice, Knockout, Multidisciplinary, genetics [Basal Metabolism], Phenotype, Area Under Curve, Diabetes Mellitus, Type 2/genetics, ddc:500, Technology Platforms, Type 2, metabolism [Triglycerides], Knockout, Science, Computational biology, Biology, genetics [Diabetes Mellitus, Type 2], General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Oxygen Consumption, Metabolic Diseases, Body Weight/genetics, Diabetes Mellitus, Genetics, Animals, Humans, Metabolic Diseases/genetics, Obesity, Gene, Gene knockout, Triglycerides, Oxygen Consumption/genetics, Blood Glucose/metabolism, genetics [Body Weight], Human Genome, Body Weight, Promoter, General Chemistry, genetics [Oxygen Consumption], High-Throughput Screening Assays, 030104 developmental biology, Diabetes Mellitus, Type 2, IMPC Consortium, lcsh:Q, Basal Metabolism, Genome-Wide Association Study
Abstract

Metabolic diseases are a worldwide problem but the underlying genetic factors and their relevance to metabolic disease remain incompletely understood. Genome-wide research is needed to characterize so-far unannotated mammalian metabolic genes. Here, we generate and analyze metabolic phenotypic data of 2016 knockout mouse strains under the aegis of the International Mouse Phenotyping Consortium (IMPC) and find 974 gene knockouts with strong metabolic phenotypes. 429 of those had no previous link to metabolism and 51 genes remain functionally completely unannotated. We compared human orthologues of these uncharacterized genes in five GWAS consortia and indeed 23 candidate genes are associated with metabolic disease. We further identify common regulatory elements in promoters of candidate genes. As each regulatory element is composed of several transcription factor binding sites, our data reveal an extensive metabolic phenotype-associated network of co-regulated genes. Our systematic mouse phenotype analysis thus paves the way for full functional annotation of the genome., The genetic basis of metabolic diseases is incompletely understood. Here, by high-throughput phenotyping of 2,016 knockout mouse strains, Rozman and colleagues identify candidate metabolic genes, many of which are associated with unexplored regulatory gene networks and metabolic traits in human GWAS.

Published
2018

165. CX3CR1–fractalkine axis drives kinetic changes of monocytes in fibrotic interstitial lung diseases

Author

Greiffo, Flavia R., primary, Viteri-Alvarez, Valeria, additional, Frankenberger, Marion, additional, Dietel, Daniela, additional, Ortega-Gomez, Almudena, additional, Lee, Joyce S., additional, Hilgendorff, Anne, additional, Behr, Jürgen, additional, Soehnlein, Oliver, additional, Eickelberg, Oliver, additional, and Fernandez, Isis E., additional

Published
2019
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166. Cigarette smoke induces overexpression of active human cathepsin S in lungs from current smokers with or without COPD

Author

Andrault, Pierre-Marie, primary, Schamberger, Andrea C., additional, Chazeirat, Thibault, additional, Sizaret, Damien, additional, Renault, Justine, additional, Staab-Weijnitz, Claudia A., additional, Hennen, Elisabeth, additional, Petit-Courty, Agnès, additional, Wartenberg, Mylène, additional, Saidi, Ahlame, additional, Baranek, Thomas, additional, Guyetant, Serge, additional, Courty, Yves, additional, Eickelberg, Oliver, additional, Lalmanach, Gilles, additional, and Lecaille, Fabien, additional

Published
2019
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170. Altered relaxation times in MRI indicate bronchopulmonary dysplasia

Author

Förster, Kai, primary, Ertl-Wagner, Birgit, additional, Ehrhardt, Harald, additional, Busen, Hannah, additional, Sass, Steffen, additional, Pomschar, Andreas, additional, Naehrlich, Lutz, additional, Schulze, Andreas, additional, Flemmer, Andreas W, additional, Hübener, Christoph, additional, Eickelberg, Oliver, additional, Theis, Fabian, additional, Dietrich, Olaf, additional, and Hilgendorff, Anne, additional

Published
2019
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172. Altered proteasome function in right ventricular hypertrophy

Author

Heitmeier, Tanja, primary, Sydykov, Akylbek, additional, Lukas, Christina, additional, Vroom, Christina, additional, Korfei, Martina, additional, Petrovic, Aleksandar, additional, Klingel, Karin, additional, Günther, Andreas, additional, Eickelberg, Oliver, additional, Weissmann, Norbert, additional, Ghofrani, Hossein Ardeschir, additional, Seeger, Werner, additional, Grimminger, Friedrich, additional, Schermuly, Ralph Theo, additional, Meiners, Silke, additional, and Kosanovic, Djuro, additional

Published
2019
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177. High-Throughput Drug Screening of ECM Deposition Inhibitors for Antifibrotic Drug Discovery

Author

Gerckens, Michael, additional, Alsafadi, Hani, additional, Wagner, Darcy, additional, Heinzelmann, Katharina, additional, Schorpp, Kenji, additional, Hadian, Kamyar, additional, Lindner, Michael, additional, Behr, Jürgen, additional, Königshoff, Melanie, additional, Eickelberg, Oliver, additional, Yildirim, Ali, additional, and Burgstaller, Gerald, additional

Published
2019
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180. Optimising experimental research in respiratory diseases: an ERS statement

Author

Bonniaud, Philippe, Fabre, Aurelie, Frossard, Nelly, Guignabert, Christophe, Inman, Mark, Kuebler, Wolfgang M., Maes, Tania, Shi, Wei, Stampfli, Martin, Uhlig, Stefan, White, Eric, Witzenrath, Martin, Bellaye, Pierre-Simon, Crestani, Bruno, Eickelberg, Oliver, Fehrenbach, Heinz, Guenther, Andreas, Jenkins, Gisli, Joos, Guy, Magnan, Antoine, Maitre, Bernard, Maus, Ulrich A., Reinhold, Petra, Vernooy, Juanita H. J., Richeldi, Luca, Kolb, Martin, Bonniaud, Philippe, Fabre, Aurelie, Frossard, Nelly, Guignabert, Christophe, Inman, Mark, Kuebler, Wolfgang M., Maes, Tania, Shi, Wei, Stampfli, Martin, Uhlig, Stefan, White, Eric, Witzenrath, Martin, Bellaye, Pierre-Simon, Crestani, Bruno, Eickelberg, Oliver, Fehrenbach, Heinz, Guenther, Andreas, Jenkins, Gisli, Joos, Guy, Magnan, Antoine, Maitre, Bernard, Maus, Ulrich A., Reinhold, Petra, Vernooy, Juanita H. J., Richeldi, Luca, and Kolb, Martin

Abstract

Experimental models are critical for the understanding of lung health and disease and are indispensable for drug development. However, the pathogenetic and clinical relevance of the models is often unclear. Further, the use of animals in biomedical research is controversial from an ethical perspective. The objective of this task force was to issue a statement with research recommendations about lung disease models by facilitating in-depth discussions between respiratory scientists, and to provide an overview of the literature on the available models. Focus was put on their specific benefits and limitations. This will result in more efficient use of resources and greater reduction in the numbers of animals employed, thereby enhancing the ethical standards and translational capacity of experimental research. The task force statement addresses general issues of experimental research (ethics, species, sex, age, ex vivo and in vitro models, gene editing). The statement also includes research recommendations on modelling asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, lung infections, acute lung injury and pulmonary hypertension. The task force stressed the importance of using multiple models to strengthen validity of results, the need to increase the availability of human tissues and the importance of standard operating procedures and data quality.

Published
2018

181. Cholesterol metabolism promotes B-cell positioning during immune pathogenesis of chronic obstructive pulmonary disease

Author

Bayram, Hasan (ORCID 0000-0002-5236-766X & YÖK ID 4890), Jia, Jie; Conlon, Thomas M.; Sarker, Rim S. J.; Tasdemir, Demet; Smirnova, Natalia F.; Srivastava, Barkha; Verleden, Stijn E.; Guneş, Gizem; Wu, Xiao; Prehn, Cornelia; Gao, Jiaqi; Heinzelmann, Katharina; Lintelmann, Jutta; Irmler, Martin; Pfeiffer, Stefan; Schloter, Michael; Zimmermann, Ralf; de Angelis, Martin Hrabe; Beckers, Johannes; Adamski, Jerzy; Eickelberg, Oliver; Yıldırım, Ali Önder, School of Medicine, Department of Pulmonology, Bayram, Hasan (ORCID 0000-0002-5236-766X & YÖK ID 4890), Jia, Jie; Conlon, Thomas M.; Sarker, Rim S. J.; Tasdemir, Demet; Smirnova, Natalia F.; Srivastava, Barkha; Verleden, Stijn E.; Guneş, Gizem; Wu, Xiao; Prehn, Cornelia; Gao, Jiaqi; Heinzelmann, Katharina; Lintelmann, Jutta; Irmler, Martin; Pfeiffer, Stefan; Schloter, Michael; Zimmermann, Ralf; de Angelis, Martin Hrabe; Beckers, Johannes; Adamski, Jerzy; Eickelberg, Oliver; Yıldırım, Ali Önder, School of Medicine, and Department of Pulmonology

Abstract

The development of chronic obstructive pulmonary disease (COPD) pathogenesis remains unclear, but emerging evidence supports a crucial role for inducible bronchus-associated lymphoid tissue (iBALT) in disease progression. Mechanisms underlying iBALT generation, particularly during chronic CS exposure, remain to be defined. Oxysterol metabolism of cholesterol is crucial to immune cell localization in secondary lymphoid tissue. Here, we demonstrate that oxysterols also critically regulate iBALT generation and the immune pathogenesis of COPD. In both COPD patients and cigarette smoke (CS)-exposed mice, we identified significantly upregulated CH25H and CYP7B1 expression in airway epithelial cells, regulating CS-induced B-cell migration and iBALT formation. Mice deficient in CH25H or the oxysterol receptor EBI2 exhibited decreased iBALT and subsequent CS-induced emphysema. Further, inhibition of the oxysterol pathway using clotrimazole resolved iBALT formation and attenuated CS-induced emphysema invivo therapeutically. Collectively, our studies are the first to mechanistically interrogate oxysterol-dependent iBALT formation in the pathogenesis of COPD, and identify a novel therapeutic target for the treatment of COPD and potentially other diseases driven by the generation of tertiary lymphoid organs., NA

Published
2018

182. A large scale hearing loss screen reveals an extensive unexplored genetic landscape for auditory dysfunction

Author

Bowl, Michael R., Simon, Michelle M., Ingham, Neil J., Greenaway, Simon, Santos, Luis, Cater, Heather, Taylor, Sarah, Mason, Jeremy, Kurbatova, Natalja, Pearson, Selina, Bower, Lynette R., Clary, Dave A., Meziane, Hamid, Reilly, Patrick, Minowa, Osamu, Kelsey, Lois, Allen, Sue, Clementson-Mobbs, Sharon, Codner, Gemma, Fray, Martin, Gardiner, Wendy, Joynson, Russell, Kenyon, Janet, Loeffler, Jorik, Nell, Barbara, Parker, Andrew, Quwailid, Deen, Stewart, Michelle, Walling, Alison, Zaman, Rumana, Chen, Chao Kung, Conte, Nathalie, Matthews, Peter, Relac, Mike, Tudose, Ilinca, Warren, Jonathan, Le Marchand, Elise, El Amri, Amal, El Fertak, Leila, Ennah, Hamid, Ali-Hadji, Dalila, Ayadi, Abdel, Wattenhofer-Donze, Marie, Moulaert, David, Jacquot, Sylvie, André, Philippe, Birling, Marie Christine, Pavlovic, Guillaume, Lalanne, Valérie, Lux, Aline, Riet, Fabrice, Mittelhaeuser, Christophe, Bour, Raphael, Guimond, Alain, Bam'Hamed, Chaouki, Leblanc, Sophie, Vasseur, Laurent, Selloum, Mohammed, Sorg, Tania, Ayabe, Shinya, Furuse, Tamio, Kaneda, Hideki, Kobayashi, Kimio, Masuya, Hiroshi, Miura, Ikuo, Obata, Yuichi, Suzuki, Tomohiro, Tamura, Masaru, Tanaka, Nobuhiko, Yamada, Ikuko, Yoshiki, Atsushi, Berberovic, Zorana, Bubshait, Mohammed, Cabezas, Jorge, Carroll, Tracy, Clark, Greg, Clarke, Shannon, Creighton, Amie, Danisment, Ozge, Eskandarian, Mohammad, Feugas, Patricia, Gertsenstein, Marina, Guo, Ruolin, Hunter, Jane, Jacob, Elsa, Lan, Qing, Laurin, Valerie, Law, Napoleon, MacMaster, Sue, Miller, David, Morikawa, Lily, Newbigging, Susan, Owen, Celeste, Penton, Patricia, Pereira, Monica, Qu, Dawei, Shang, Xueyuan, Sleep, Gillian, Sohel, Khondoker, Tondat, Sandra, Wang, Yanchun, Vukobradovic, Igor, Zhu, Yingchun, Chiani, Francesco, Di Pietro, Chiara, Di Segni, Gianfranco, Ermakova, Olga, Ferrara, Filomena, Fruscoloni, Paolo, Gambadoro, Aalessia, Gastaldi, Serena, Golini, Elisabetta, Sala, Gina La, Mandillo, Silvia, Marazziti, Daniela, Massimi, Marzia, Matteoni, Rafaele, Orsini, Tiziana, Pasquini, Miriam, Raspa, Marcello, Rauch, Aline, Rossi, Gianfranco, Rossi, Nicoletta, Putti, Sabrina, Scavizzi, Ferdinando, Tocchini-Valentini, Giuseppe D., Beig, Joachim, Bürger, Antje, Giesert, Florian, Graw, Jochen, Kühn, Ralf, Oritz, Oskar, Schick, Joel, Seisenberger, Claudia, Amarie, Oana, Garrett, Lillian, Hölter, Sabine M., Zimprich, Annemarie, Aguilar-Pimentel, Antonio, Beckers, Johannes, Brommage, Robert, Calzada-Wack, Julia, Fuchs, Helmut, Gailus-Durner, Valérie, Lengger, Christoph, Leuchtenberger, Stefanie, Maier, Holger, Marschall, Susan, Moreth, Kristin, Neff, Frauke, Östereicher, Manuela A., Rozman, Jan, Steinkamp, Ralph, Stoeger, Claudia, Treise, Irina, Stoeger, Tobias, Yildrim, Ali Önder, Eickelberg, Oliver, Becker, Lore, Klopstock, Thomas, Ollert, Markus, Busch, Dirk H., Schmidt-Weber, Carsten, Bekeredjian, Raffi, Zimmer, Andreas, Rathkolb, Birgit, Wolf, Eckhard, Klingenspor, Martin, Tocchini-Valentini, Glauco P., Gao, Xiang, Bradley, Allan, Skarnes, William C., Moore, Mark, Beaudet, Arthur L., Justice, Monica J., Seavitt, John, Dickinson, Mary E., Wurst, Wolfgang, De Angelis, Martin Hrabe, Herault, Yann, Wakana, Shigeharu, Nutter, Lauryl M.J., Flenniken, Ann M., McKerlie, Colin, Murray, Stephen A., Svenson, Karen L., Braun, Robert E., West, David B., Lloyd, K. C.Kent, Adams, David J., White, Jacqui, Karp, Natasha, Flicek, Paul, Smedley, Damian, Meehan, Terrence F., Parkinson, Helen E., Teboul, Lydia M., Wells, Sara, Steel, Karen P., Mallon, Ann Marie, Brown, Steve D.M., Mason, Jeremy [0000-0002-2796-5123], de Angelis, Martin Hrabe [0000-0002-7898-2353], Herault, Yann [0000-0001-7049-6900], Wakana, Shigeharu [0000-0001-8532-0924], McKerlie, Colin [0000-0002-2232-0967], Lloyd, KC Kent [0000-0002-5318-4144], Flicek, Paul [0000-0002-3897-7955], Smedley, Damian [0000-0002-5836-9850], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, Cancer Research, Candidate gene, General Physics and Astronomy, Datasets as Topic, Mice, 2.1 Biological and endogenous factors, Protein Interaction Maps, Aetiology, lcsh:Science, Pediatric, Genetics, Mice, Knockout, Multidisciplinary, medicine.diagnostic_test, Hearing Tests, Ear, Phenotype, medicine.anatomical_structure, Technology Platforms, International Mouse Phenotyping Consortium, medicine.symptom, Biotechnology, Hearing Loss/epidemiology, Hearing loss, Knockout, 1.1 Normal biological development and functioning, Science, Biology, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Clinical Research, Underpinning research, medicine, otorhinolaryngologic diseases, Auditory system, Animals, Genetic Testing, IMPC, mouse, auditory dysfunction, Set (psychology), Hearing Loss, Gene, Genetic testing, Auditory dysfunction, Human Genome, General Chemistry, 030104 developmental biology, Protein Interaction Maps/genetics, lcsh:Q
Abstract

The developmental and physiological complexity of the auditory system is likely reflected in the underlying set of genes involved in auditory function. In humans, over 150 non-syndromic loci have been identified, and there are more than 400 human genetic syndromes with a hearing loss component. Over 100 non-syndromic hearing loss genes have been identified in mouse and human, but we remain ignorant of the full extent of the genetic landscape involved in auditory dysfunction. As part of the International Mouse Phenotyping Consortium, we undertook a hearing loss screen in a cohort of 3006 mouse knockout strains. In total, we identify 67 candidate hearing loss genes. We detect known hearing loss genes, but the vast majority, 52, of the candidate genes were novel. Our analysis reveals a large and unexplored genetic landscape involved with auditory function., The full extent of the genetic basis for hearing impairment is unknown. Here, as part of the International Mouse Phenotyping Consortium, the authors perform a hearing loss screen in 3006 mouse knockout strains and identify 52 new candidate genes for genetic hearing loss.

Published
2017

183. Additional file 1: Figure S1. of Nanoparticle exposure reactivates latent herpesvirus and restores a signature of acute infection

Author

Sattler, Christine, Moritz, Franco, Shanze Chen, Steer, Beatrix, Kutschke, David, Irmler, Martin, Beckers, Johannes, Eickelberg, Oliver, Schmitt-Kopplin, Philippe, Adler, Heiko, and Stoeger, Tobias

Abstract

Average Size and size distribution of the used NP. Figure S2. Measurement of cell viability. Figure S3. Exposure to NP reactivates lytic virus in persistently infected cells in vitro in a dose dependent manner. Figure S4. Exposure to NP reactivates lytic virus in persistently infected cells independently of the particle aspect ratio. Figure S5. Short-time exposure of latently infected mice to NP differentially regulates gene expression in whole lung tissue cells independently of the particle aspect ratio. Figure S6. Confirmation of gene expression data by real-time quantitative PCR for selected genes. Figure S7. Exposure of latently infected mice to CNP leads to an increase in glycerophospholipids. Figure S8. Exposure of latently infected mice to DWCNT leads to an increase in glycerophospholipids. Figure S9. Exposure of persistently infected cells to TiO2 NP or DEP has differential effects on virus reactivation in vitro. Table S1. Gene expression values of selected genes (PDF 1767Â kb)

Published
2017
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184. Female mice lacking Pald1 exhibit endothelial cell apoptosis and emphysema

Author

Egaña, Isabel, Kaito, Hiroshi, Klopstock, Thomas, Fuchs, Helmut, Gailus-Durner, Valerie, Hrabe de Angelis, Martin, Rask-Andersen, Helge, Johansson, Henrik J, Lehtiö, Janne, He, Liqun, Yildirim, Ali Ö, Hellström, Mats, Nitzsche, Anja, Consortium, German Mouse Clinic, Aguilar-Pimentel, Antonio, Ollert, Markus, Schmidt-Weber, Carsten, Amarie, Oana, Graw, Jochen, Beckers, Johannes, Garrett, Lillian, Hölter, Sabine M, Zimprich, Annemarie, Becker, Lore, Wurst, Wolfgang, Moreth, Kristin, Bekeredjian, Raffi, Neff, Frauke, Calzada-Wack, Julia, Rácz, Ildikó, Zimmer, Andreas, Rathkolb, Birgit, Wolf, Eckhard, Rozman, Jan, Ballester-Lopez, Carolina, Klingenspor, Martin, Stoeger, Tobias, Eickelberg, Oliver, Treise, Irina, Busch, Dirk H, Östereicher, Manuela, Steinkamp, Ralph, Lengger, Christoph, Maier, Holger, Stoeger, Claudia, Niaudet, Colin, Leuchtenberger, Stefanie, Petkova, Milena, Liu, Wei, Vanlandewijck, Michael, and Vernaleken, Alexandra

Subjects
Male, Heterozygote, lcsh:Medicine, Apoptosis, genetics [Emphysema], pathology [Endothelial Cells], Article, genetics [Phosphoprotein Phosphatases], Mice, Sex Factors, Phosphoprotein Phosphatases, Animals, Humans, lcsh:Science, Pald1 protein, mouse, Lung, pathology [Emphysema], metabolism [Phosphoprotein Phosphatases], Emphysema, Mice, Knockout, lcsh:R, growth & development [Endothelium, Vascular], Endothelial Cells, Embryo, Mammalian, Mice, Inbred C57BL, Disease Models, Animal, physiology [Apoptosis], lcsh:Q, Female, Endothelium, Vascular, blood supply [Lung], ddc:600
Abstract

Paladin (Pald1, mKIAA1274 or x99384) was identified in screens for vascular-specific genes and is a putative phosphatase. Paladin has also been proposed to be involved in various biological processes such as insulin signaling, innate immunity and neural crest migration. To determine the role of paladin we have now characterized the Pald1 knock-out mouse in a broad array of behavioral, physiological and biochemical tests. Here, we show that female, but not male, Pald1 heterozygous and homozygous knock-out mice display an emphysema-like histology with increased alveolar air spaces and impaired lung function with an obstructive phenotype. In contrast to many other tissues where Pald1 is restricted to the vascular compartment, Pald1 is expressed in both the epithelial and mesenchymal compartments of the postnatal lung. However, in Pald1 knock-out females, there is a specific increase in apoptosis and proliferation of endothelial cells, but not in non-endothelial cells. This results in a transient reduction of endothelial cells in the maturing lung. Our data suggests that Pald1 is required during lung vascular development and for normal function of the developing and adult lung in a sex-specific manner. To our knowledge, this is the first report of a sex-specific effect on endothelial cell apoptosis.

Published
2017

185. Altered proteasome function in right ventricular hypertrophy.

Author

Heitmeier, Tanja, Sydykov, Akylbek, Lukas, Christina, Vroom, Christina, Korfei, Martina, Petrovic, Aleksandar, Klingel, Karin, Günther, Andreas, Eickelberg, Oliver, Weissmann, Norbert, Ghofrani, Hossein Ardeschir, Seeger, Werner, Grimminger, Friedrich, Schermuly, Ralph Theo, Meiners, Silke, and Kosanovic, Djuro

Subjects
RIGHT ventricular hypertrophy, BORTEZOMIB, CARDIAC hypertrophy, PULMONARY artery, PROTEASOME inhibitors, PROTEOLYSIS
Abstract

Aims In patients with pulmonary hypertension, right ventricular hypertrophy (RVH) is a detrimental condition that ultimately results in right heart failure and death. The ubiquitin proteasome system has been identified as a major protein degradation system to regulate cardiac remodelling in the left heart. Its role in right heart hypertrophy, however, is still ambiguous. Methods and results RVH was induced in mice by pulmonary artery banding (PAB). Both, expression and activity of the proteasome was found to be up-regulated in the hypertrophied right ventricle (RV) compared to healthy controls. Catalytic inhibition of the proteasome by the two proteasome inhibitors Bortezomib (BTZ) and ONX-0912 partially improved RVH both in preventive and therapeutic applications. Native gel analysis revealed that specifically the 26S proteasome complexes were activated in experimental RVH. Increased assembly of 26S proteasomes was accompanied by elevated expression of Rpn6, a rate-limiting subunit of 26S proteasome assembly, in hypertrophied cardiomyocytes of the right heart. Intriguingly, patients with RVH also showed increased expression of Rpn6 in hypertrophied cardiomyocytes of the RV as identified by immunohistochemical staining. Conclusion Our data demonstrate that alterations in expression and activity of proteasomal subunits play a critical role in the development of RVH. Moreover, this study provides an improved understanding on the selective activation of the 26S proteasome in RVH that might be driven by the rate-limiting subunit Rpn6. In RVH, Rpn6 therefore represents a more specific target to interfere with proteasome function than the commonly used catalytic proteasome inhibitors. [ABSTRACT FROM AUTHOR]

Published
2020
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186. Altered relaxation times in MRI indicate bronchopulmonary dysplasia.

Author

Förster, Kai, Ertl Wagner, Birgit, Ehrhardt, Harald, Busen, Hannah, Sass, Steffen, Pomschar, Andreas, Naehrlich, Lutz, Schulze, Andreas, Flemmer, Andreas W., Hübener, Christoph, Eickelberg, Oliver, Theis, Fabian, Dietrich, Olaf, and Hilgendorff, Anne

Subjects
BRONCHOPULMONARY dysplasia, PULMONARY function tests, PREMATURE infants, RELAXATION for health, LOGISTIC regression analysis
Abstract

We developed a MRI protocol using transverse (T2) and longitudinal (T1) mapping sequences to characterise lung structural changes in preterm infants with bronchopulmonary dysplasia (BPD). We prospectively enrolled 61 infants to perform 3-Tesla MRI of the lung in quiet sleep. Statistical analysis was performed using logistic Group Lasso regression and logistic regression. Increased lung T2 relaxation time and decreased lung T1 relaxation time indicated BPD yielding an area under the curve (AUC) of 0.80. Results were confirmed in an independent study cohort (AUC 0.75) and mirrored by lung function testing, indicating the high potential for MRI in future BPD diagnostics. TRIAL REGISTRATION: DRKS00004600. [ABSTRACT FROM AUTHOR]

Published
2020
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187. Cell-surface phenotyping identifies CD36 and CD97 as novel markers of fibroblast quiescence in lung fibrosis

Author

Heinzelmann, Katharina, primary, Lehmann, Mareike, additional, Gerckens, Michael, additional, Noskovičová, Nina, additional, Frankenberger, Marion, additional, Lindner, Michael, additional, Hatz, Rudolf, additional, Behr, Jürgen, additional, Hilgendorff, Anne, additional, Königshoff, Melanie, additional, and Eickelberg, Oliver, additional

Published
2018
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188. Cigarette smoke induces overexpression of cathepsin S in active smokers with and without COPD

Author

Wartenberg, Mylène, primary, Andrault, Pierre-Marie, additional, Schamberger, Andrea C., additional, Chazeirat, Thibault, additional, Sizaret, Damien, additional, Renault, Justine, additional, Petit, Agnès, additional, Saidi, Ahlame, additional, Guyetant, Serge, additional, Courty, Yves, additional, Eickelberg, Oliver, additional, Lalmanach, Gilles, additional, and Lecaille, Fabien, additional

Published
2018
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193. Upregulation and Nuclear Location of MMP28 in Alveolar Epithelium of Idiopathic Pulmonary Fibrosis

Author

Maldonado, Mariel, primary, Salgado-Aguayo, Alfonso, additional, Herrera, Iliana, additional, Cabrera, Sandra, additional, Ortíz-Quintero, Blanca, additional, Staab-Weijnitz, Claudia A., additional, Eickelberg, Oliver, additional, Ramírez, Remedios, additional, Manicone, Anne M., additional, Selman, Moisés, additional, and Pardo, Annie, additional

Published
2018
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194. An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics

Author

Angelidis, Ilias, primary, Simon, Lukas M., additional, Fernandez, Isis E., additional, Strunz, Maximilian, additional, Mayr, Christoph H., additional, Greiffo, Flavia R., additional, Tsitsiridis, George, additional, Graf, Elisabeth, additional, Strom, Tim-Matthias, additional, Eickelberg, Oliver, additional, Mann, Matthias, additional, Theis, Fabian J., additional, and Schiller, Herbert B., additional

Published
2018
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195. Intrauterine smoke exposure deregulates lung function, pulmonary transcriptomes, and in particular insulin-like growth factor (IGF)-1 in a sex-specific manner

Author

Dehmel, Stefan, primary, Nathan, Petra, additional, Bartel, Sabine, additional, El-Merhie, Natalia, additional, Scherb, Hagen, additional, Milger, Katrin, additional, John-Schuster, Gerrit, additional, Yildirim, Ali Oender, additional, Hylkema, Machteld, additional, Irmler, Martin, additional, Beckers, Johannes, additional, Schaub, Bianca, additional, Eickelberg, Oliver, additional, and Krauss-Etschmann, Susanne, additional

Published
2018
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197. Optimising experimental research in respiratory diseases: an ERS statement

Author

Bonniaud, Philippe, primary, Fabre, Aurélie, additional, Frossard, Nelly, additional, Guignabert, Christophe, additional, Inman, Mark, additional, Kuebler, Wolfgang M., additional, Maes, Tania, additional, Shi, Wei, additional, Stampfli, Martin, additional, Uhlig, Stefan, additional, White, Eric, additional, Witzenrath, Martin, additional, Bellaye, Pierre-Simon, additional, Crestani, Bruno, additional, Eickelberg, Oliver, additional, Fehrenbach, Heinz, additional, Guenther, Andreas, additional, Jenkins, Gisli, additional, Joos, Guy, additional, Magnan, Antoine, additional, Maitre, Bernard, additional, Maus, Ulrich A., additional, Reinhold, Petra, additional, Vernooy, Juanita H.J., additional, Richeldi, Luca, additional, and Kolb, Martin, additional

Published
2018
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200. Early Identification of Bronchopulmonary Dysplasia Using Novel Biomarkers by Proteomic Screening

Author

Förster, Kai, primary, Sass, Steffen, additional, Ehrhardt, Harald, additional, Mous, Daphne S., additional, Rottier, Robbert J., additional, Oak, Prajakta, additional, Schulze, Andreas, additional, Flemmer, Andreas W., additional, Gronbach, Judith, additional, Hübener, Christoph, additional, Desai, Tushar, additional, Eickelberg, Oliver, additional, Theis, Fabian J., additional, and Hilgendorff, Anne, additional

Published
2018
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