34 results on '"Capece, Vincenzo"'
Search Results
2. Innate immune memory in the brain shapes neurological disease hallmarks
- Author
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Wendeln, Ann-Christin, Degenhardt, Karoline, Kaurani, Lalit, Gertig, Michael, Ulas, Thomas, Jain, Gaurav, Wagner, Jessica, Häsler, Lisa M., Wild, Katleen, Skodras, Angelos, Blank, Thomas, Staszewski, Ori, Datta, Moumita, Centeno, Tonatiuh Pena, Capece, Vincenzo, Islam, Md. Rezaul, Kerimoglu, Cemil, Staufenbiel, Matthias, Schultze, Joachim L., Beyer, Marc, Prinz, Marco, Jucker, Mathias, Fischer, André, and Neher, Jonas J.
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- 2018
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3. Swiss public health measures associated with reduced SARS-CoV-2 transmission using genome data
- Author
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Nadeau, Sarah A, Vaughan, Timothy G, Beckmann, Christiane; https://orcid.org/0000-0001-9030-083X, Topolsky, Ivan; https://orcid.org/0000-0002-7561-0810, Chen, Chaoran; https://orcid.org/0000-0002-8763-2937, Hodcroft, Emma; https://orcid.org/0000-0002-0078-2212, Schär, Tobias, Nissen, Ina, Santacroce, Natascha, Burcklen, Elodie, Ferreira, Pedro; https://orcid.org/0000-0003-0559-6125, Jablonski, Kim Philipp; https://orcid.org/0000-0002-4166-4343, Posada-Céspedes, Susana; https://orcid.org/0000-0002-7459-8186, Capece, Vincenzo, Seidel, Sophie; https://orcid.org/0000-0002-4484-9888, Santamaria de Souza, Noemi; https://orcid.org/0000-0001-7134-7480, Martinez-Gomez, Julia M; https://orcid.org/0000-0002-5684-3707, Cheng, Phil; https://orcid.org/0000-0003-2940-006X, Bosshard, Philipp P; https://orcid.org/0000-0002-1154-2281, Levesque, Mitchell P; https://orcid.org/0000-0001-5902-9420, Kufner, Verena; https://orcid.org/0000-0003-4233-5952, Schmutz, Stefan; https://orcid.org/0000-0002-1955-7007, Zaheri, Maryam; https://orcid.org/0000-0003-2777-835X, Huber, Michael; https://orcid.org/0000-0002-0384-0000, Trkola, Alexandra; https://orcid.org/0000-0003-1013-876X, Cordey, Samuel; https://orcid.org/0000-0002-2684-5680, Laubscher, Florian; https://orcid.org/0000-0002-8803-981X, Gonçalves, Ana Rita; https://orcid.org/0000-0002-7893-0158, Aeby, Sébastien; https://orcid.org/0000-0001-9726-7438, Pillonel, Trestan; https://orcid.org/0000-0002-5725-7929, et al, Nadeau, Sarah A, Vaughan, Timothy G, Beckmann, Christiane; https://orcid.org/0000-0001-9030-083X, Topolsky, Ivan; https://orcid.org/0000-0002-7561-0810, Chen, Chaoran; https://orcid.org/0000-0002-8763-2937, Hodcroft, Emma; https://orcid.org/0000-0002-0078-2212, Schär, Tobias, Nissen, Ina, Santacroce, Natascha, Burcklen, Elodie, Ferreira, Pedro; https://orcid.org/0000-0003-0559-6125, Jablonski, Kim Philipp; https://orcid.org/0000-0002-4166-4343, Posada-Céspedes, Susana; https://orcid.org/0000-0002-7459-8186, Capece, Vincenzo, Seidel, Sophie; https://orcid.org/0000-0002-4484-9888, Santamaria de Souza, Noemi; https://orcid.org/0000-0001-7134-7480, Martinez-Gomez, Julia M; https://orcid.org/0000-0002-5684-3707, Cheng, Phil; https://orcid.org/0000-0003-2940-006X, Bosshard, Philipp P; https://orcid.org/0000-0002-1154-2281, Levesque, Mitchell P; https://orcid.org/0000-0001-5902-9420, Kufner, Verena; https://orcid.org/0000-0003-4233-5952, Schmutz, Stefan; https://orcid.org/0000-0002-1955-7007, Zaheri, Maryam; https://orcid.org/0000-0003-2777-835X, Huber, Michael; https://orcid.org/0000-0002-0384-0000, Trkola, Alexandra; https://orcid.org/0000-0003-1013-876X, Cordey, Samuel; https://orcid.org/0000-0002-2684-5680, Laubscher, Florian; https://orcid.org/0000-0002-8803-981X, Gonçalves, Ana Rita; https://orcid.org/0000-0002-7893-0158, Aeby, Sébastien; https://orcid.org/0000-0001-9726-7438, Pillonel, Trestan; https://orcid.org/0000-0002-5725-7929, and et al
- Abstract
Genome sequences from evolving infectious pathogens allow quantification of case introductions and local transmission dynamics. We sequenced 11,357 severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genomes from Switzerland in 2020 - the sixth largest effort globally. Using a representative subset of these data, we estimated viral introductions to Switzerland and their persistence over the course of 2020. We contrasted these estimates with simple null models representing the absence of certain public health measures. We show that Switzerland's border closures de-coupled case introductions from incidence in neighboring countries. Under a simple model, we estimate an 86-98% reduction in introductions during Switzerland's strictest border closures. Furthermore, the Swiss 2020 partial lockdown roughly halved the time for sampled introductions to die out. Last, we quantified local transmission dynamics once introductions into Switzerland occurred, using a phylodynamic model. We found that transmission slowed 35-63% upon outbreak detection in summer 2020, but not in fall. This finding may indicate successful contact tracing over summer before overburdening in fall. The study highlights the added value of genome sequencing data for understanding transmission dynamics.
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- 2023
4. Swiss public health measures associated with reduced SARS-CoV-2 transmission using genome data
- Author
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Nadeau, Sarah A., primary, Vaughan, Timothy G., additional, Beckmann, Christiane, additional, Topolsky, Ivan, additional, Chen, Chaoran, additional, Hodcroft, Emma, additional, Schär, Tobias, additional, Nissen, Ina, additional, Santacroce, Natascha, additional, Burcklen, Elodie, additional, Ferreira, Pedro, additional, Jablonski, Kim Philipp, additional, Posada-Céspedes, Susana, additional, Capece, Vincenzo, additional, Seidel, Sophie, additional, Santamaria de Souza, Noemi, additional, Martinez-Gomez, Julia M., additional, Cheng, Phil, additional, Bosshard, Philipp P., additional, Levesque, Mitchell P., additional, Kufner, Verena, additional, Schmutz, Stefan, additional, Zaheri, Maryam, additional, Huber, Michael, additional, Trkola, Alexandra, additional, Cordey, Samuel, additional, Laubscher, Florian, additional, Gonçalves, Ana Rita, additional, Aeby, Sébastien, additional, Pillonel, Trestan, additional, Jacot, Damien, additional, Bertelli, Claire, additional, Greub, Gilbert, additional, Leuzinger, Karoline, additional, Stange, Madlen, additional, Mari, Alfredo, additional, Roloff, Tim, additional, Seth-Smith, Helena, additional, Hirsch, Hans H., additional, Egli, Adrian, additional, Redondo, Maurice, additional, Kobel, Olivier, additional, Noppen, Christoph, additional, du Plessis, Louis, additional, Beerenwinkel, Niko, additional, Neher, Richard A., additional, Beisel, Christian, additional, and Stadler, Tanja, additional
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- 2023
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5. Oasis 2: improved online analysis of small RNA-seq data
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Rahman, Raza-Ur, Gautam, Abhivyakti, Bethune, Jörn, Sattar, Abdul, Fiosins, Maksims, Magruder, Daniel Sumner, Capece, Vincenzo, Shomroni, Orr, and Bonn, Stefan
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- 2018
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6. HDAC inhibitor-dependent transcriptome and memory reinstatement in cognitive decline models
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Benito, Eva, Urbanke, Hendrik, Ramachandran, Binu, Barth, Jonas, Halder, Rashi, Awasthi, Ankit, Jain, Gaurav, Capece, Vincenzo, Burkhardt, Susanne, Navarro-Sala, Magdalena, Nagarajan, Sankari, Schutz, Anna- Lena, Johnsen, Steven A., Bonn, Stefan, Luhrmann, Reinhardt, Dean, Camin, and Fischer, Andre
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Gene expression -- Analysis -- Models -- Research ,Transferases ,Cognition disorders ,Health care industry - Abstract
Aging and increased amyloid burden are major risk factors for cognitive diseases such as Alzheimer's disease (AD). Effective therapies for these diseases are lacking. Here, we evaluated mouse models of age- associated memory impairment and amyloid deposition to study transcriptome and cell type-specific epigenome plasticity in the brain and peripheral organs. We determined that aging and amyloid pathology are associated with inflammation and impaired synaptic function in the hippocampal CA1 region as the result of epigenetic-dependent alterations in gene expression. In both amyloid and aging models, inflammation was associated with increased gene expression linked to a subset of transcription factors, while plasticity gene deregulation was differentially mediated. Amyloid pathology impaired histone acetylation and decreased expression of plasticity genes, while aging altered H4K12 acetylation- linked differential splicing at the intron-exon junction in neurons, but not nonneuronal cells. Furthermore, oral administration of the clinically approved histone deacetylase inhibitor vorinostat not only restored spatial memory, but also exerted antiinflammatory action and reinstated epigenetic balance and transcriptional homeostasis at the level of gene expression and exon usage. This study provides a systems-level investigation of transcriptome plasticity in the hippocampal CA1 region in aging and AD models and suggests that histone deacetylase inhibitors should be further explored as a cost-effective therapeutic strategy against age-associated cognitive decline., Introduction Epigenetic processes, including posttranslational modifications of histones, regulate gene-expression programs and play a key role in genome-environment interactions (1, 2). Recent data suggest that histone acetylation regulates memory consolidation [...]
- Published
- 2015
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7. Swiss public health measures associated with reduced SARS-CoV-2 transmission using genome data
- Author
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Nadeau, Sarah A., primary, Vaughan, Timothy G., additional, Beckmann, Christiane, additional, Topolsky, Ivan, additional, Chen, Chaoran, additional, Hodcroft, Emma, additional, Schär, Tobias, additional, Nissen, Ina, additional, Santacroce, Natascha, additional, Burcklen, Elodie, additional, Ferreira, Pedro, additional, Jablonski, Kim Philipp, additional, Posada-Céspedes, Susana, additional, Capece, Vincenzo, additional, Seidel, Sophie, additional, de Souza, Noemi Santamaria, additional, Martinez-Gomez, Julia M., additional, Cheng, Phil, additional, Bosshard, Philipp P., additional, Levesque, Mitchell P., additional, Kufner, Verena, additional, Schmutz, Stefan, additional, Zaheri, Maryam, additional, Huber, Michael, additional, Trkola, Alexandra, additional, Cordey, Samuel, additional, Laubscher, Florian, additional, Gonçalves, Ana Rita, additional, Aeby, Sébastien, additional, Pillonel, Trestan, additional, Jacot, Damien, additional, Bertelli, Claire, additional, Greub, Gilbert, additional, Leuzinger, Karoline, additional, Stange, Madlen, additional, Mari, Alfredo, additional, Roloff, Tim, additional, Seth-Smith, Helena, additional, Hirsch, Hans H., additional, Egli, Adrian, additional, Redondo, Maurice, additional, Kobel, Olivier, additional, Noppen, Christoph, additional, du Plessis, Louis, additional, Beerenwinkel, Niko, additional, Neher, Richard A., additional, Beisel, Christian, additional, and Stadler, Tanja, additional
- Published
- 2021
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8. H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion
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Kerimoglu, Cemil, primary, Pham, Linh, additional, Tonchev, Anton B., additional, Sakib, M. Sadman, additional, Xie, Yuanbin, additional, Sokpor, Godwin, additional, Ulmke, Pauline Antonie, additional, Kaurani, Lalit, additional, Abbas, Eman, additional, Nguyen, Huong, additional, Rosenbusch, Joachim, additional, Michurina, Alexandra, additional, Capece, Vincenzo, additional, Angelova, Meglena, additional, Maricic, Nenad, additional, Brand-Saberi, Beate, additional, Esgleas, Miriam, additional, Albert, Mareike, additional, Minkov, Radoslav, additional, Kovachev, Emil, additional, Teichmann, Ulrike, additional, Seong, Rho H., additional, Huttner, Wieland B., additional, Nguyen, Huu Phuc, additional, Stoykova, Anastassia, additional, Staiger, Jochen F., additional, Fischer, Andre, additional, and Tuoc, Tran, additional
- Published
- 2021
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9. H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion by activating TRNP1 expression
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Kerimoglu, Cemil, primary, Pham, Linh, additional, Tonchev, Anton B., additional, Sakib, M. Sadman, additional, Xie, Yuanbin, additional, Sokpor, Godwin, additional, Ulmke, Pauline Antonie, additional, Kaurani, Lalit, additional, Abbas, Eman, additional, Nguyen, Huong, additional, Rosenbusch, Joachim, additional, Michurina, Alexandra, additional, Capece, Vincenzo, additional, Angelova, Meglena, additional, Esgleas, Miriam, additional, Albert, Mareike, additional, Minkov, Radoslav, additional, Kovachev, Emil, additional, Teichmann, Ulrike, additional, Seong, Rho H., additional, Huttner, Wieland, additional, Götz, Magdalena, additional, Nguyen, Huu Phuc, additional, Stoykova, Anastassia, additional, Staiger, Jochen F., additional, Fischer, Andre, additional, and Tuoc, Tran, additional
- Published
- 2021
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10. Within-patient genetic diversity of SARS-CoV-2
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Kuipers, Jack, Batavia, Aashil A., Jablonski, Kim Philipp, Bayer, Fritz, Borgsmüller, Nico, Dondi, Arthur, Drăgan, Monica-Andreea, Ferreira, Pedro, Jahn, Katharina, Lamberti, Lisa, Pirkl, Martin, Posada Cespedes, Susana, Topolsky, Ivan, Nissen, Ina, Santacroce, Natascha, Burcklen, Elodie, Schär, Tobias, Capece, Vincenzo, Beckmann, Christiane, Kobel, Olivier, Noppen, Christoph, Redondo, Maurice, Nadeau, Sarah Ann, Seidel, Sophie, Santamaria de Souza, Noemie, Beisel, Christian, Stadler, Tanja, and Beerenwinkel, Niko
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respiratory system ,human activities - Abstract
SARS-CoV-2, the virus responsible for the current COVID-19 pandemic, is evolving into different genetic variants by accumulating mutations as it spreads globally. In addition to this diversity of consensus genomes across patients, RNA viruses can also display genetic diversity within individual hosts, and co-existing viral variants may affect disease progression and the success of medical interventions. To systematically examine the intra-patient genetic diversity of SARS-CoV-2, we processed a large cohort of 3939 publicly-available deeply sequenced genomes with specialised bioinformatics software, along with 749 recently sequenced samples from Switzerland. We found that the distribution of diversity across patients and across genomic loci is very unbalanced with a minority of hosts and positions accounting for much of the diversity. For example, the D614G variant in the Spike gene, which is present in the consensus sequences of 67.4% of patients, is also highly diverse within hosts, with 29.7% of the public cohort being affected by this coexistence and exhibiting different variants. We also investigated the impact of several technical and epidemiological parameters on genetic heterogeneity and found that age, which is known to be correlated with poor disease outcomes, is a significant predictor of viral genetic diversity., bioRxiv
- Published
- 2020
11. Quantifying SARS-CoV-2 spread in Switzerland based on genomic sequencing data
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Nadeau, Sarah Ann, Beckmann, Christiane, Topolsky, Ivan, Vaughan, Timothy, Hodcroft, Emma, Schär, Tobias, Nissen, Ina, Santacroce, Natascha, Burcklen, Elodie, Ferreira, Pedro, Jablonski, Kim Philipp, Posada Cespedes, Susana, Capece, Vincenzo, Seidel, Sophie, Santamaria de Souza, Noemi, Martinez-Gomez, Julia M., Cheng, Phil, Bosshard, Philipp P., Levesque, Mitchell P., Kufner, Verena, Schmutz, Stefan, Zaheri, Maryam, Huber, Michael, Trkola, Alexandra, Cordey, Samuel, Laubscher, Florian, Gonçalves, Ana Rita, Leuzinger, Karoline, Stange, Madlen, Mari, Alfredo, Roloff, Tim, Seth-Smith, Helena, Hirsch, Hans H., Egli, Adrian, Redondo, Maurice, Kobel, Oliver, Noppen, Christoph, Beerenwinkel, Niko, Neher, Richard A., Beisel, Christian, and Stadler, Tanja
- Abstract
Pathogen genomes provide insights into their evolution and epidemic spread. We sequenced 1,439 SARS-CoV-2 genomes from Switzerland, representing 3-7% of all confirmed cases per week. Using these data, we demonstrate that no one lineage became dominant, pointing against evolution towards general lower virulence. On an epidemiological level, we report no evidence of cryptic transmission before the first confirmed case. We find many early viral introductions from Germany, France, and Italy and many recent introductions from Germany and France. Over the summer, we quantify the number of non-traceable infections stemming from introductions, quantify the effective reproductive number, and estimate the degree of undersampling. Our framework can be applied to quantify evolution and epidemiology in other locations or for other pathogens based on genomic data., medRxiv
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- 2020
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12. Quantifying SARS-CoV-2 spread in Switzerland based on genomic sequencing data
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Nadeau, Sarah, primary, Beckmann, Christiane, additional, Topolsky, Ivan, additional, Vaughan, Timothy, additional, Hodcroft, Emma, additional, Schär, Tobias, additional, Nissen, Ina, additional, Santacroce, Natascha, additional, Burcklen, Elodie, additional, Ferreira, Pedro, additional, Jablonski, Kim Philipp, additional, Posada-Céspedes, Susana, additional, Capece, Vincenzo, additional, Seidel, Sophie, additional, de Souza, Noemi Santamaria, additional, Martinez-Gomez, Julia M., additional, Cheng, Phil, additional, Bosshard, Philipp P., additional, Levesque, Mitchell P., additional, Kufner, Verena, additional, Schmutz, Stefan, additional, Zaheri, Maryam, additional, Huber, Michael, additional, Trkola, Alexandra, additional, Cordey, Samuel, additional, Laubscher, Florian, additional, Gonçalves, Ana Rita, additional, Leuzinger, Karoline, additional, Stange, Madlen, additional, Mari, Alfredo, additional, Roloff, Tim, additional, Seth-Smith, Helena, additional, Hirsch, Hans H., additional, Egli, Adrian, additional, Redondo, Maurice, additional, Kobel, Olivier, additional, Noppen, Christoph, additional, Beerenwinkel, Niko, additional, Neher, Richard A., additional, Beisel, Christian, additional, and Stadler, Tanja, additional
- Published
- 2020
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13. Within-patient genetic diversity of SARS-CoV-2
- Author
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Kuipers, Jack, primary, Batavia, Aashil A, additional, Jablonski, Kim Philipp, additional, Bayer, Fritz, additional, Borgsmüller, Nico, additional, Dondi, Arthur, additional, Drăgan, Monica-Andreea, additional, Ferreira, Pedro, additional, Jahn, Katharina, additional, Lamberti, Lisa, additional, Pirkl, Martin, additional, Posada-Céspedes, Susana, additional, Topolsky, Ivan, additional, Nissen, Ina, additional, Santacroce, Natascha, additional, Burcklen, Elodie, additional, Schär, Tobias, additional, Capece, Vincenzo, additional, Beckmann, Christiane, additional, Kobel, Olivier, additional, Noppen, Christoph, additional, Redondo, Maurice, additional, Nadeau, Sarah, additional, Seidel, Sophie, additional, Santamaria de Souza, Noemie, additional, Beisel, Christian, additional, Stadler, Tanja, additional, and Beerenwinkel, Niko, additional
- Published
- 2020
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14. Changes in m6A RNA methylation contribute to heart failure progression by modulating translation
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Berulava, Tea, primary, Buchholz, Eric, additional, Elerdashvili, Vakhtang, additional, Pena, Tonatiuh, additional, Islam, Md Rezaul, additional, Lbik, Dawid, additional, Mohamed, Belal A., additional, Renner, Andre, additional, von Lewinski, Dirk, additional, Sacherer, Michael, additional, Bohnsack, Katherine E., additional, Bohnsack, Markus T., additional, Jain, Gaurav, additional, Capece, Vincenzo, additional, Cleve, Nicole, additional, Burkhardt, Susanne, additional, Hasenfuss, Gerd, additional, Fischer, Andre, additional, and Toischer, Karl, additional
- Published
- 2019
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15. Additional file 1: of Oasis 2: improved online analysis of small RNA-seq data
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Raza-Ur Rahman, Abhivyakti Gautam, Jรถrn Bethune, Sattar, Abdul, Fiosins, Maksims, Magruder, Daniel, Capece, Vincenzo, Orr Shomroni, and Bonn, Stefan
- Abstract
Oasis2-Suppl-Material.docx: This file contains supplementary material and figures as well. (DOCX 125 kb)
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- 2018
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16. Organ-specific small non-coding RNA responses in domestic (Sudani) ducks experimentally infected with highly pathogenic avian influenza virus (H5N1)
- Author
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Samir, Mohamed, primary, Vidal, Ramon O., additional, Abdallah, Fatma, additional, Capece, Vincenzo, additional, Seehusen, Frauke, additional, Geffers, Robert, additional, Hussein, Ashraf, additional, Ali, Ahmed A. H., additional, Bonn, Stefan, additional, and Pessler, Frank, additional
- Published
- 2019
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17. Alpha-synuclein deregulates the expression of COL4A2 and impairs ER-Golgi function
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Paiva, Isabel, Jain, Garav, Lázaro, Diana F, Gotovac Jerčić, Kristina, Hentrich, Thomas, Kerimoglu, Cemil, Pinho, Raquel, M. Szegő, Eva, Burkhardt, Susanne, Capece, Vincenzo, Halder, Rashi, Islam, Rezaul, Xylaki, Mary, A. Caldi Gomes, Lucas, Roser, Anna-Elisa, Lingor, Paul, M. Schulze-Hentrich, Julia, Borovečki, Fran, Fischer, Andre, F. Outeiro, Tiago, Paiva, Isabel, Jain, Garav, Lázaro, Diana F, Gotovac Jerčić, Kristina, Hentrich, Thomas, Kerimoglu, Cemil, Pinho, Raquel, M. Szegő, Eva, Burkhardt, Susanne, Capece, Vincenzo, Halder, Rashi, Islam, Rezaul, Xylaki, Mary, A. Caldi Gomes, Lucas, Roser, Anna-Elisa, Lingor, Paul, M. Schulze-Hentrich, Julia, Borovečki, Fran, Fischer, Andre, and F. Outeiro, Tiago
- Published
- 2018
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18. Changes in m6A RNA methylation contribute to heart failure progression by modulating translation.
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Berulava, Tea, Buchholz, Eric, Elerdashvili, Vakhtang, Pena, Tonatiuh, Islam, Md Rezaul, Lbik, Dawid, Mohamed, Belal A., Renner, Andre, Lewinski, Dirk, Sacherer, Michael, Bohnsack, Katherine E., Bohnsack, Markus T., Jain, Gaurav, Capece, Vincenzo, Cleve, Nicole, Burkhardt, Susanne, Hasenfuss, Gerd, Fischer, Andre, Toischer, Karl, and von Lewinski, Dirk
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RNA methylation ,GENETIC translation ,HEART failure ,CARDIAC hypertrophy ,NUCLEOTIDE sequencing ,RNA metabolism ,RESEARCH ,ANIMAL experimentation ,RESEARCH methodology ,RNA ,EVALUATION research ,COMPARATIVE studies ,METHYLATION ,GENES ,RESEARCH funding ,MICE - Abstract
Aims: Deregulation of epigenetic processes and aberrant gene expression are important mechanisms in heart failure. Here we studied the potential relevance of m6A RNA methylation in heart failure development.Methods and Results: We analysed m6A RNA methylation via next-generation sequencing. We found that approximately one quarter of the transcripts in the healthy mouse and human heart exhibit m6A RNA methylation. During progression to heart failure we observed that changes in m6A RNA methylation exceed changes in gene expression both in mouse and human. RNAs with altered m6A RNA methylation were mainly linked to metabolic and regulatory pathways, while changes in RNA expression level mainly represented changes in structural plasticity. Mechanistically, we could link m6A RNA methylation to altered RNA translation and protein production. Interestingly, differentially methylated but not differentially expressed RNAs showed differential polysomal occupancy, indicating transcription-independent modulation of translation. Furthermore, mice with a cardiomyocyte restricted knockout of the RNA demethylase Fto exhibited an impaired cardiac function compared to control mice.Conclusions: We could show that m6A landscape is altered in heart hypertrophy and heart failure. m6A RNA methylation changes lead to changes in protein abundance, unconnected to mRNA levels. This uncovers a new transcription-independent mechanisms of translation regulation. Therefore, our data suggest that modulation of epitranscriptomic processes such as m6A methylation might be an interesting target for therapeutic interventions. [ABSTRACT FROM AUTHOR]- Published
- 2020
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19. Organ-specific small non-coding RNA responses in domestic (Sudani) ducks experimentally infected with highly pathogenic avian influenza virus (H5N1).
- Author
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Samir, Mohamed, Vidal, Ramon O., Abdallah, Fatma, Capece, Vincenzo, Seehusen, Frauke, Geffers, Robert, Hussein, Ashraf, Ali, Ahmed A. H., Bonn, Stefan, and Pessler, Frank
- Abstract
The duck represents an important reservoir of influenza viruses for transmission to other avian and mammalian hosts, including humans. The increased pathogenicity of the recently emerging clades of highly pathogenic avian influenza (HPAI) viruses of the H5N1 subtype in ducks features systemic viral spread and organ-to-organ variation in viral transcription and tissue damage. We previously reported that experimental infection of Sudani ducks (Cairina moschata) with an Egyptian HPAI (H5N1) virus (clade 2.2.1.2) features high viral replication and severe tissue damage in lung, but lower viral replication and only mild histological changes in brain. Little is known about the involvement of miRNA in organ-specific responses to H5N1 viruses in ducks, and involvement of the other classes of small noncoding RNA (sncRNA) has not been investigated so far. Following RNA sequencing, we have annotated the duck sncRNome and compared global expression changes of the four major sncRNA classes (miRNAs, piRNAs, snoRNAs, snRNAs) between duck lung and brain during a 120 h time course of infection with this HPAI strain. We find major organ-specific differences in miRNA, piRNA and snoRNA populations even before infection and substantial reprogramming of all sncRNA classes throughout infection, which was less pronounced in brain. Pathway prediction analysis of miRNA targets revealed enrichment of inflammation-, infection- and apoptosis-related pathways in lung, but enrichment of metabolism-related pathways (including tryptophan metabolism) in brain. Thus, organ-specific differences in sncRNA responses may contribute to differences in viral replication and organ damage in ducks infected with isolates from this emerging HPAI clade, and likely other strains. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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20. Alpha-synuclein deregulates the expression of COL4A2 and impairs ER-Golgi function
- Author
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Paiva, Isabel, primary, Jain, Gaurav, additional, Lázaro, Diana F., additional, Jerčić, Kristina Gotovac, additional, Hentrich, Thomas, additional, Kerimoglu, Cemil, additional, Pinho, Raquel, additional, Szegő, Èva M., additional, Burkhardt, Susanne, additional, Capece, Vincenzo, additional, Halder, Rashi, additional, Islam, Rezaul, additional, Xylaki, Mary, additional, Caldi Gomes, Lucas A., additional, Roser, Anna-Elisa, additional, Lingor, Paul, additional, Schulze-Hentrich, Julia M., additional, Borovečki, Fran, additional, Fischer, André, additional, and Outeiro, Tiago F., additional
- Published
- 2018
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21. RNA-Dependent Intergenerational Inheritance of Enhanced Synaptic Plasticity after Environmental Enrichment
- Author
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Benito, Eva, primary, Kerimoglu, Cemil, additional, Ramachandran, Binu, additional, Pena-Centeno, Tonatiuh, additional, Jain, Gaurav, additional, Stilling, Roman Manuel, additional, Islam, Md Rezaul, additional, Capece, Vincenzo, additional, Zhou, Qihui, additional, Edbauer, Dieter, additional, Dean, Camin, additional, and Fischer, André, additional
- Published
- 2018
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22. KMT2A and KMT2B Mediate Memory Function by Affecting Distinct Genomic Regions
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Kerimoglu, Cemil, Sakib, M. Sadman, Jain, Gaurav, Benito, Eva, Burkhardt, Susanne, Capece, Vincenzo, Kaurani, Lalit, Halder, Rashi, Carlos Agı´s-Balboa, Roberto, Stilling, Roman, Urbanke, Hendrik, Kranz, Andrea, Stewart, A. Francis, Fiascher, Andre, Kerimoglu, Cemil, Sakib, M. Sadman, Jain, Gaurav, Benito, Eva, Burkhardt, Susanne, Capece, Vincenzo, Kaurani, Lalit, Halder, Rashi, Carlos Agı´s-Balboa, Roberto, Stilling, Roman, Urbanke, Hendrik, Kranz, Andrea, Stewart, A. Francis, and Fiascher, Andre
- Published
- 2017
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23. P113: Of mice and men – a direct comparison of signaling in pressureoverload induced hypertrophy and failure
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Vidal, Ramon, Capece, Vincenzo, Fischer, Andre, and Bonn, Stefan
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ddc:610 - Abstract
Purpose: It is still largely unknown, if signaling in the heart in response to pressure overload is conserved in patients and mouse models.The aim of this study is to compare signaling in human biopsies withpressure overload induced compensated hypertrophy (CH) and “mild”failure (HF) to the transverse aortic constriction (TAC) mouse-model ofCH and HF. Using transcriptomics and computational tools we received for the fi rst time a highly comparative data-set comprising expression profi les, signaling pathways and microRNAome changes atdiff erent stages after pressure overload in human and mouse.
- Published
- 2016
24. Endophilin-A Deficiency Induces the Foxo3a-Fbxo32 Network in the Brain and Causes Dysregulation of Autophagy and the Ubiquitin-Proteasome System
- Author
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Murdoch, John D., Rostosky, Christine M., Gowrisankaran, Sindhuja, Arora, Amandeep S., Soukup, Sandra-Fausia, Vidal, Ramon, Capece, Vincenzo, Freytag, Siona, Fischer, Andre, Verstreken, Patrik, Bonn, Stefan, Raimundo, Nuno, and Milosevic, Ira
- Subjects
Male ,Aging ,genetics [SKP Cullin F-Box Protein Ligases] ,Transcription, Genetic ,Muscle Proteins ,Apoptosis ,metabolism [Hippocampus] ,genetics [Muscle Proteins] ,Hippocampus ,pathology [Ataxia] ,metabolism [Forkhead Box Protein O3] ,genetics [Homeostasis] ,Mice ,pathology [Aging] ,genetics [Parkinson Disease] ,metabolism [Ubiquitin] ,complications [Movement Disorders] ,Fbxo32 protein, mouse ,Homeostasis ,lcsh:QH301-705.5 ,Mice, Knockout ,protein homeostasis ,Movement Disorders ,Forkhead Box Protein O3 ,neurodegeneration ,Brain ,pathology [Nerve Degeneration] ,Parkinson Disease ,genetics [Ataxia] ,metabolism [Autophagosomes] ,Up-Regulation ,metabolism [Acyltransferases] ,Protein Binding ,Proteasome Endopeptidase Complex ,autophagy ,metabolism [Muscle Proteins] ,FBXO32 protein, human ,genetics [Mutation] ,Article ,FBXO32 ,endophilin ,Autophagy ,deficiency [Acyltransferases] ,Animals ,Humans ,endocytosis ,FoxO3 protein, mouse ,ddc:610 ,metabolism [Proteasome Endopeptidase Complex] ,SKP Cullin F-Box Protein Ligases ,Endophilin-A ,Ubiquitin-Proteasome System ,Ubiquitin ,ataxia ,Autophagosomes ,metabolism [SKP Cullin F-Box Protein Ligases] ,pathology [Movement Disorders] ,pathology [Parkinson Disease] ,complications [Nerve Degeneration] ,pathology [Hippocampus] ,lcsh:Biology (General) ,metabolism [Brain] ,Mutation ,Nerve Degeneration ,Parkinson’s disease ,genetics [Forkhead Box Protein O3] ,2-acylglycerophosphate acyltransferase ,next-generation sequencing ,ubiquitin-proteasome system ,Acyltransferases ,HeLa Cells - Abstract
Summary Endophilin-A, a well-characterized endocytic adaptor essential for synaptic vesicle recycling, has recently been linked to neurodegeneration. We report here that endophilin-A deficiency results in impaired movement, age-dependent ataxia, and neurodegeneration in mice. Transcriptional analysis of endophilin-A mutant mice, complemented by proteomics, highlighted ataxia- and protein-homeostasis-related genes and revealed upregulation of the E3-ubiquitin ligase FBXO32/atrogin-1 and its transcription factor FOXO3A. FBXO32 overexpression triggers apoptosis in cultured cells and neurons but, remarkably, coexpression of endophilin-A rescues it. FBXO32 interacts with all three endophilin-A proteins. Similarly to endophilin-A, FBXO32 tubulates membranes and localizes on clathrin-coated structures. Additionally, FBXO32 and endophilin-A are necessary for autophagosome formation, and both colocalize transiently with autophagosomes. Our results point to a role for endophilin-A proteins in autophagy and protein degradation, processes that are impaired in their absence, potentially contributing to neurodegeneration and ataxia., Graphical Abstract, Highlights • Endophilin-A is needed for autophagosome formation in mammalian neurons and brain • Absence of endophilin-A upregulates the E3-ubiquitin ligase FBXO32 • FBXO32-endophilin-A interaction maintains neuronal health and protein homeostasis • Endophilin-A KO mice show age-dependent ataxia, motor impairments, and neurodegeneration, Regulation of protein homeostasis and autophagy has become a promising line of research in the neurodegeneration field. Murdoch et al. now find that endophilin-A, a key factor in clathrin-mediated endocytosis, regulates protein homeostasis through the Foxo3a-Fbxo32 network.
- Published
- 2016
25. RNA-dependent intergenerational inheritance of enhanced synaptic plasticity after environmental enrichment
- Author
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Benito, Eva, primary, Kerimoglu, Cemil, additional, Ramachandran, Binu, additional, Zhou, Qihui, additional, Pena, Tonatiuh, additional, Capece, Vincenzo, additional, Jain, Gaurav, additional, Burkhardt, Susanne, additional, Stilling, Roman, additional, Edbauer, Dieter, additional, Dean, Camin, additional, and Fischer, André, additional
- Published
- 2017
- Full Text
- View/download PDF
26. Oasis2.0: improved online analysis of small RNA-seq data
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Rahman, Raza-Ur, primary, Gautam, Abhivyakti, additional, Bethune, Jörn, additional, Sattar, Abdul, additional, Fiosins, Maksims, additional, Magruder, Daniel Sumner, additional, Capece, Vincenzo, additional, Shomroni, Orr, additional, and Bonn, Stefan, additional
- Published
- 2017
- Full Text
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27. KMT2A and KMT2B Mediate Memory Function by Affecting Distinct Genomic Regions
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Kerimoglu, Cemil, primary, Sakib, M. Sadman, additional, Jain, Gaurav, additional, Benito, Eva, additional, Burkhardt, Susanne, additional, Capece, Vincenzo, additional, Kaurani, Lalit, additional, Halder, Rashi, additional, Agís-Balboa, Roberto Carlos, additional, Stilling, Roman, additional, Urbanke, Hendrik, additional, Kranz, Andrea, additional, Stewart, A. Francis, additional, and Fischer, Andre, additional
- Published
- 2017
- Full Text
- View/download PDF
28. Integration of deep sequencing data reveals global regulation of gene expression in human cardiac hypertrophy and heart failure by differential methylation, hydroxymethylation and microRNA expression
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Halder, Rashi, Vidal, Ramon, Capece, Vincenzo, Bonn, Stefan, and Fischer, Andre
- Subjects
ddc:610 - Abstract
Purpose: Many pathways and genes involved in hypertrophy and heart failurehave been described in animal models, but how the transition from compensatoryhypertrophy to heart failure is initiated in humans remains unclear. This study aimsto identify global mechanisms of gene regulation in the human heart in responseto biomechanical stress (pressure overload) by analyzing the transcriptomes and comparing the contribution of methylation, hydroxymethylation and ncRNAs inaortic stenosis patients with two disease conditions: compensatory hypertrophy(normal ejection fraction) and heart failure (reduced ejection fraction).Methods: DNA and RNA were extracted from snap frozen human myocar-dial biopsy samples and RNA-sequencing (RNA-seq), methylated DNAimmunoprecipitation-sequencing (MeDIP-seq), hydroxymethylated DNAimmunoprecipitation-sequencing (hMeDIP-seq) and smallRNA-sequencing(smallRNA-seq) was carried out using deep HiSeq high throughput sequenc-ing. By comparing the patients’ data to control samples without heart disease usingve replicates for each group and experiment, differentially expressed genes, differ-entially methylated regions, hydroxymethylated regions and differentially expressedmicroRNAs were identied.Results: As expected, the transcriptomes show a high degree of deregulation.Transcriptionfactor (TF) network analysis suggests that approximately 20% ofcondition specic differential expression might be a result of TF regulation. Whilethe methylome is slightly changed in both conditions, the hydroxymethylome ismassively changed in heart failure suggesting a regulatory contribution to thefailing hypertrophic phenotype. Furthermore, differential expression of microRNAsis increased in heart failure and network and target analysis suggests that almost allcandidates are involved in the regulation of differentially expressed genes in both,the compensatory hypertrophy group and heart failure group.Conclusion: The data presented here suggest a regulatory contribution of hydrox-ymethylation and the regulation by microRNAs during the transition of humancompensatory hypertrophy to heart failure.
- Published
- 2015
29. Endophilin-A Deficiency Induces the Foxo3a-Fbxo32 Network in the Brain and Causes Dysregulation of Autophagy and the Ubiquitin-Proteasome System
- Author
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Murdoch, John D., primary, Rostosky, Christine M., additional, Gowrisankaran, Sindhuja, additional, Arora, Amandeep S., additional, Soukup, Sandra-Fausia, additional, Vidal, Ramon, additional, Capece, Vincenzo, additional, Freytag, Siona, additional, Fischer, Andre, additional, Verstreken, Patrik, additional, Bonn, Stefan, additional, Raimundo, Nuno, additional, and Milosevic, Ira, additional
- Published
- 2016
- Full Text
- View/download PDF
30. DNA methylation changes in plasticity genes accompany the formation and maintenance of memory
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Halder, Rashi, Hennion, Magali, Vidal, Ramon, Shomroni, Orr, Rahaman, Raza-Ur, Rajput, Ashish, Pena Centeno, Tonatiuh, van Bebber, Frauke, Capece, Vincenzo, Garcia Vizcaino, Julio, Schuetz, Anna-Lena, Burkhardt, Susanne, Benito, Eva, Navarro Sala, Magdalena, Bahari Javan, Sanaz, Haass, Christian, Schmid, Bettina, Fischer, Andre, Bonn, Stefan, Halder, Rashi, Hennion, Magali, Vidal, Ramon, Shomroni, Orr, Rahaman, Raza-Ur, Rajput, Ashish, Pena Centeno, Tonatiuh, van Bebber, Frauke, Capece, Vincenzo, Garcia Vizcaino, Julio, Schuetz, Anna-Lena, Burkhardt, Susanne, Benito, Eva, Navarro Sala, Magdalena, Bahari Javan, Sanaz, Haass, Christian, Schmid, Bettina, Fischer, Andre, and Bonn, Stefan
- Published
- 2015
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31. DNA methylation changes in plasticity genes accompany the formation and maintenance of memory
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Halder, Rashi, primary, Hennion, Magali, additional, Vidal, Ramon O, additional, Shomroni, Orr, additional, Rahman, Raza-Ur, additional, Rajput, Ashish, additional, Centeno, Tonatiuh Pena, additional, van Bebber, Frauke, additional, Capece, Vincenzo, additional, Vizcaino, Julio C Garcia, additional, Schuetz, Anna-Lena, additional, Burkhardt, Susanne, additional, Benito, Eva, additional, Sala, Magdalena Navarro, additional, Javan, Sanaz Bahari, additional, Haass, Christian, additional, Schmid, Bettina, additional, Fischer, Andre, additional, and Bonn, Stefan, additional
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- 2015
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- View/download PDF
32. Oasis: online analysis of small RNA deep sequencing data
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Capece, Vincenzo, primary, Garcia Vizcaino, Julio C., additional, Vidal, Ramon, additional, Rahman, Raza-Ur, additional, Pena Centeno, Tonatiuh, additional, Shomroni, Orr, additional, Suberviola, Irantzu, additional, Fischer, Andre, additional, and Bonn, Stefan, additional
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- 2015
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33. De-regulation of gene expression and alternative splicing affects distinct cellular pathways in the aging hippocampus
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Stilling, Roman M., primary, Benito, Eva, additional, Barth, Jonas, additional, Gertig, Michael, additional, Capece, Vincenzo, additional, Burckhardt, Susanne, additional, Bonn, Stefan, additional, and Fischer, Andre, additional
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- 2014
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34. DNA methylation changes in plasticity genes accompany the formation and maintenance of memory
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Halder, Rashi, Hennion, Magali, Vidal, Ramon O, Shomroni, Orr, Rahman, Raza-Ur, Rajput, Ashish, Centeno, Tonatiuh Pena, van Bebber, Frauke, Capece, Vincenzo, Vizcaino, Julio C Garcia, Schuetz, Anna-Lena, Burkhardt, Susanne, Benito, Eva, Sala, Magdalena Navarro, Javan, Sanaz Bahari, Haass, Christian, Schmid, Bettina, Fischer, Andre, and Bonn, Stefan
- Abstract
The ability to form memories is a prerequisite for an organism's behavioral adaptation to environmental changes. At the molecular level, the acquisition and maintenance of memory requires changes in chromatin modifications. In an effort to unravel the epigenetic network underlying both short- and long-term memory, we examined chromatin modification changes in two distinct mouse brain regions, two cell types and three time points before and after contextual learning. We found that histone modifications predominantly changed during memory acquisition and correlated surprisingly little with changes in gene expression. Although long-lasting changes were almost exclusive to neurons, learning-related histone modification and DNA methylation changes also occurred in non-neuronal cell types, suggesting a functional role for non-neuronal cells in epigenetic learning. Finally, our data provide evidence for a molecular framework of memory acquisition and maintenance, wherein DNA methylation could alter the expression and splicing of genes involved in functional plasticity and synaptic wiring.
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- 2016
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