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Document Type
- Article (5)
Language
- English (5)
Has Fulltext
- yes (5)
Is part of the Bibliography
- no (5)
Keywords
- Long non-coding RNAs (2)
- long non-coding RNA (2)
- Angiogenesis (1)
- Apoptosis (1)
- Cardiology (1)
- G3BP1 (1)
- Histone post-translational modifications (1)
- RNA turnover (1)
- alternative splicing (1)
- gene expression (1)
- nonsense-mediated mRNA decay (1)
- tight junctions (1)
- vascular integrity (1)
Institute
Trembinski, Dorotée Julia ; Bink, Diewertje I. ; Theodorou, Kosta ; Sommer, Janina ; Fischer, Ariane ; Bergen, Anke van ; Kuo, Chao-Chung ; Costa, Ivan G. ; Schürmann, Christoph ; Leisegang, Matthias ; Brandes, Ralf ; Alekseeva, Tijna ; Brill, Boris ; Wietelmann, Astrid ; Johnson, Christopher N. ; Spring-Connell, Alexander ; Kaulich, Manuel ; Werfel, Stanislas ; Engelhardt, Stefan ; Hirt, Marc Nikolaus ; Yorgan, Kaja ; Eschenhagen, Thomas ; Kirchhof, Luisa ; Hofmann, Patrick ; Jaé, Nicolas Christopher ; Wittig, Ilka ; Hamdani, Nazha ; Bischof, Corinne ; Krishnan, Jaya ; Houtkooper, Riekelt H. ; Dimmeler, Stefanie ; Boon, Reinier
Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes. Importantly, loss of SARRAH (OXCT1-AS1) in human engineered heart tissue results in impaired contractile force development. SARRAH directly binds to the promoters of genes downregulated after SARRAH silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix forming domain of Sarrah show an increase in apoptosis. One of the direct SARRAH targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability. Overexpression of Sarrah in mice shows better recovery of cardiac contractile function after AMI compared to control mice. In summary, we identified the anti-apoptotic evolutionary conserved lncRNA Sarrah, which is downregulated by aging, as a regulator of cardiomyocyte survival.
Long-range angular correlations on the near and away side in p–Pb collisions at √sNN=5.02 TeV
(2013)
Abelev, Betty ; Adam, Jaroslav ; Adamová, Dagmar ; Marshall Adare, Andrew ; Aggarwal, Madan Mohan ; Aglieri Rinella, Gianluca ; Agnello, Michelangelo ; Gabor Agocs, Andras ; Agostinelli, Andrea ; Ahammed, Zubayer ; Ahmad, Nazeer ; Ahmad, Arshad ; Ahn, Sul-Ah ; Ahn, Sang Un ; Ajaz, Muhammad ; Akindinov, Alexander ; Aleksandrov, Dmitry ; Alessandro, Bruno ; Alici, Andrea ; Alkin, Anton ; Jonathan Almaraz Avina, Erick ; Alme, Johan ; Alt, Torsten ; Altini, Valerio ; Altinpinar, Sedat ; Altsybeev, Igor ; Andrei, Cristian ; Andronic, Anton ; Anguelov, Venelin ; Anielski, Jonas ; Daniel Anson, Christopher ; Antičić, Tome ; Antinori, Federico ; Antonioli, Pietro ; Aphecetche, Laurent Bernard ; Appelshäuser, Harald ; Arbor, Nicolas ; Arcelli, Silvia ; Arend, Andreas ; Armesto, Nestor ; Arnaldi, Roberta ; Robert Aronsson, Tomas ; Arsene, Ionut Cristian ; Arslandok, Mesut ; Asryan, Andzhey ; Augustinus, Andre ; Averbeck, Ralf Peter ; Awes, Terry ; Heikki Aysto, Juha ; Danish Azmi, Mohd ; Jakob Bach, Matthias ; Badalà, Angela ; Baek, Yong Wook ; Bailhache, Raphaëlle ; Bala, Renu ; Baldini Ferroli, Rinaldo ; Baldisseri, Alberto ; Baltasar Dos Santos Pedrosa, Fernando ; Ban, Jaroslav ; Chandra Baral, Rama ; Barbera, Roberto ; Barile, Francesco ; Barnaföldi, Gergely Gábor ; Stuart Barnby, Lee ; Barret, Valerie ; Gustaw Bartke, Jerzy ; Basile, Maurizio ; Bastid, Nicole ; Basu, Sumit ; Bathen, Bastian ; Batigne, Guillaume ; Batyunya, Boris ; Heinrich Baumann, Christoph ; Gardner Bearden, Ian ; Beck, Hans ; Kumar Behera, Nirbhay ; Belikov, Iouri ; Bellini, Francesca ; Bellwied, Rene ; Belmont-Moreno, Ernesto ; Bencédi, Gyula ; Beolè, Stefania ; Berceanu, Ionela ; Bercuci, Alexandru ; Berdnikov, Yaroslav ; Berényi, Dániel ; Annick Erica Bergognon, Anais ; Berzano, Dario ; Betev, Latchezar ; Bhasin, Anju ; Kumar Bhati, Ashok ; Bhom, Jihyun ; Bianchi, Livio ; Bianchi, Nicola ; Bielčík, Jaroslav ; Bielčíková, Jana ; Bilandzic, Ante ; Bjelogrlic, Sandro ; Blanco, Francesco ; Blanco, Fernando ; Blau, Dmitry S. ; Blume, Christoph ; Boccioli, Marco ; Boettger, Stefan ; Bogdanov, Alexey A. ; Bøggild, Hans ; Bogolyubsky, Mikhail ; Boldizsar, Laszlo ; Bombara, Marek ; Book, Julian ; Borel, Herve ; Borissov, Alexander ; Bossú, Francesco ; Botje, Michiel ; Botta, Elena ; Braidot, Ermes ; Braun-Munzinger, Peter ; Bregant, Marco ; Breitner, Timo Gunther ; Alexander Broker, Theo ; Allen Browning, Tyler ; Broz, Michal ; Brun, Rene ; Bruna, Elena ; Eugenio Bruno, Giuseppe ; Budnikov, Dmitry ; Büsching, Henner ; Bufalino, Stefania ; Bunčić, Predrag ; Busch, Oliver ; Buthelezi, Edith Zinhle ; Caballero Orduna, Diego ; Caffarri, Davide ; Cai, Xu ; Caines, Helen Louise ; Calvo Villar, Ernesto ; Camerini, Paolo ; Canoa Roman, Veronica ; Cara Romeo, Giovanni ; Carena, Wisla ; Carena, Francesco ; Carlin Filho, Nelson ; Carminati, Federico ; Ofelia Casanova Diaz, Amaya ; Castillo Castellanos, Javier Ernesto ; Castillo Hernández, Juan Francisco ; Anna Rita Casula, Ester ; Catanescu, Vasile ; Cavicchioli, Costanza ; Ceballos Sanchez, Cesar ; Čepila, Jan ; Cerello, Piergiaio ; Chang, Beomsu ; Chapeland, Sylvain ; Fernand Charvet, Jean-Luc ; Chattopadhyay, Sukalyan ; Chattopadhyay, Subhasis ; Chawla, Isha ; Gerard Cherney, Michael ; Cheshkov, Cvetan ; Cheynis, Brigitte ; Miguel Chibante Barroso, Vasco ; Chinellato, David Dobrigkeit ; Chochula, Peter ; Chojnacki, Marek ; Choudhury, Subikash ; Christakoglou, Panagiotis ; Christensen, Christian Holm ; Christiansen, Peter L. ; Chujo, Tatsuya ; Chung, Suh-Urk ; Cicalò, Corrado ; Cifarelli, Luisa ; Cindolo, Federico ; Willy Andre Cleymans, Jean ; Coccetti, Fabrizio ; Colamaria, Fabio Filippo ; Colella, Domenico ; Collu, Alberto ; Conesa Balbastre, Gustavo ; Conesa del Valle, Zaida ; Elizabeth Connors, Megan ; Contin, Giacomo ; Contreras Nuno, Jesus Guillermo ; Cormier, Thomas Michael ; Corrales Morales, Yasser ; Cortese, Pietro ; Cortes Maldonado, Ismael ; Rogerio Cosentino, Mauro ; Costa, Filippo ; Enrique Cotallo, Manuel ; Crescio, Elisabetta ; Crochet, Philippe ; Cruz Alaniz, Emilia ; Cruz Albino, Rigoberto ; Cuautle, Eleazar ; Cunqueiro Mendez, Leticia ; Dainese, Andrea ; Dalsgaard, Hans Hjersing ; Danu, Andrea ; Das, Indranil ; Das, Debasish ; Das, Supriya ; Das, Kushal ; Kumar Dash, Ajay ; Dash, Sadhana ; De, Sudipan ; de Barros, Gabriel ; De Caro, Annalisa ; De Cataldo, Giacinto ; Cuveland, Jan de ; De Falco, Alessandro ; De Gruttola, Daniele ; Delagrange, Hugues ; Deloff, Andrzej ; De Marco, Nora ; Denes, Ervin ; De Pasquale, Salvatore ; Deppman, Airton ; DʼErasmo, Ginevra ; Stefan de Rooij, Raoul ; Angel Diaz Corchero, Miguel ; Di Bari, Domenico ; Dietel, Thomas ; Di Giglio, Carmelo ; Di Liberto, Sergio ; Di Mauro, Antonio ; Di Nezza, Pasquale ; Divià, Roberto ; Djuvsland, Øystein ; Florin Dobrin, Alexandru ; Antoni Dobrowolski, Tadeusz ; Donigus, Benjamin ; Dordic, Olja ; Driga, Olga ; Kumar Dubey, Anand ; Dubla, Andrea ; Ducroux, Laurent ; Dupieux, Pascal ; Dutta Majumdar, A.K. ; Elia, Domenico ; Philip Emschermann, David ; Engel, Heiko ; Erazmus, Barbara ; Austrheim Erdal, Hege ; Espagnon, Bruno ; Danielle Estienne, Magali ; Esumi, ShinIchi ; Evans, David ; Eyyubova, Gyulnara ; Fabris, Daniela ; Faivre, Julien ; Falchieri, Davide ; Fantoni, Alessandra ; Fasel, Markus ; Worsley Fearick, Roger ; Fehlker, Dominik ; Feldkamp, Linus ; Felea, Daniel ; Feliciello, Alessandro ; Fenton-Olsen, Bo ; Feofilov, Grigory ; Fernández Téllez, Arturo ; Ferretti, Alessandro ; Festanti, Andrea ; Figiel, Jan ; Figueredo, Marcel ; Filchagin, Sergey ; Finogeev, Dmitry ; Fionda, Fiorella Maria Celeste ; Enrichetta, Maria Fiore ; Floratos, Emmanuel ; Floris, Michele ; Foertsch, Siegfried Valentin ; Foka, Panagiota ; Fokin, Sergey ; Fragiacomo, Enrico ; Francescon, Andrea ; Michael Frankenfeld, Ulrich ; Fuchs, Ulrich ; Furget, Christophe ; Fusco Girard, Mario ; Gaardhøje, Jens Jørgen ; Gagliardi, Martino ; Gago Medina, Alberto Martín ; Gallio, Mauro ; Gangadharan, Dhevan Raja ; Ganoti, Paraskevi ; Garabatos Cuadrado, Jose Maria ; Garcia-Solis, Edmundo ; Garishvili, Irakli ; Gerhard, Jochen ; Germain, Marie ; Geuna, Claudio ; Gheata, Mihaela ; Gheata, Andrei George ; Ghidini, Bruno ; Ghosh, Premomoy ; Gianotti, Paola ; Robert Girard, Martin ; Giubellino, Paolo ; Gładysz-Dziaduś, Ewa ; Glässel, Peter ; Gomez, Ramon ; Gonzalez Ferreiro, Elena ; Helena Gonzalez-Trueba, Laura ; González Zamora, Pedro ; Gorbunov, Sergey ; Goswami, Ankita ; Gotovac, Sven ; Graczykowski, Łukasz Kamil ; Grajcarek, Robert ; Grelli, Alessandro ; Grigoraș, Costin ; Gabriela Grigoras, Alina ; Grigoriev, Vladislav A. ; Grigoryan, Ara ; Grigoryan, Smbat ; Grinyov, Boris ; Grion, Nevio ; Gros, Philippe ; Große-Oetringhaus, Jan Fiete ; Grossiord, Jean-Yves ; Grosso, Raffaele ; Guber, Fedor ; Guernane, Rachid ; Guerzoni, Barbara ; Rene Joseph Guilbaud, Maxime ; Herlache Gulbrandsen, Kristjan ; Gulkanyan, Hrant ; Gunji, Taku ; Gupta, Anik ; Gupta, Ramni ; Haake, Rüdiger ; Senneset Haaland, Oystein ; Marie Hadjidakis, Cynthia ; Haiduc, Maria ; Hamagaki, Hideki ; Hamar, Gergö ; Han, Byounghee ; David Hanratty, Luke ; Hansen, Alexander ; Harmanova, Zuzana ; William Harris, John ; Hartig, Matthias ; Harton, Austin ; Hatzifotiadou, Despoina ; Hayashi, Shinichi ; Hayrapetyan, Arsen ; Heckel, Stefan Thomas ; Ansgar Heide, Markus ; Helstrup, Håvard ; Ionut Herghelegiu, Andrei ; Antonio Herrera Corral, Gerardo ; Herrmann, Norbert ; Hess, Benjamin Andreas ; Hetland, Kristin Fanebust ; Hicks, Bernard ; Hippolyte, Boris ; Hori, Yasuto ; Zahariev Hristov, Peter ; Hrivnacova, Ivana ; Huang, Meidana ; Humanic, Thomas J. ; Sung Hwang, Dae ; Ichou, Raphaelle ; Ilkaev, Radiy ; Ilkiv, Iryna ; Inaba, Motoi ; Incani, Elisa ; Giaio Innocenti, Pier ; Michele Innocenti, Gian ; Ippolitov, Mikhail ; Irfan, Muhammad ; Geae Ivan, Cristian ; Ivanov, Vladimir ; Ivanov, Andrey ; Ivanov, Marian ; Ivanytskyi, Oleksii ; Wlodzimierz Jacholkowski, Adam ; Jacobs, Peter ; Jin Jang, Haeng ; Anna Janik, Malgorzata ; Janik, Rudolf ; Jayarathna, Sandun ; Jena, Satyajit ; Manu Jha, Deeptanshu ; Tonatiuh Jimenez Bustamante, Raul ; 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Angular correlations between charged trigger and associated particles are measured by the ALICE detector in p–Pb collisions at a nucleon–nucleon centre-of-mass energy of 5.02 TeV for transverse momentum ranges within 0.5<pT,assoc<pT,trig<4 GeV/c. The correlations are measured over two units of pseudorapidity and full azimuthal angle in different intervals of event multiplicity, and expressed as associated yield per trigger particle. Two long-range ridge-like structures, one on the near side and one on the away side, are observed when the per-trigger yield obtained in low-multiplicity events is subtracted from the one in high-multiplicity events. The excess on the near-side is qualitatively similar to that recently reported by the CMS Collaboration, while the excess on the away-side is reported for the first time. The two-ridge structure projected onto azimuthal angle is quantified with the second and third Fourier coefficients as well as by near-side and away-side yields and widths. The yields on the near side and on the away side are equal within the uncertainties for all studied event multiplicity and pT bins, and the widths show no significant evolution with event multiplicity or pT. These findings suggest that the near-side ridge is accompanied by an essentially identical away-side ridge.
Kirchhof, Luisa ; Fouani, Youssef ; Knau, Andrea ; Aslan, Galip S. ; Heumüller, Andreas ; Wittig, Ilka ; Müller-McNicoll, Michaela ; Dimmeler, Stefanie ; Jaé, Nicolas Christopher
Besides transcription, RNA decay accounts for a large proportion of regulated gene expression and is paramount for cellular functions. Classical RNA surveillance pathways, like nonsense-mediated decay (NMD), are also implicated in the turnover of non-mutant transcripts. Whereas numerous protein factors have been assigned to distinct RNA decay pathways, the contribution of long non-coding RNAs (lncRNAs) to RNA turnover remains unknown. Here we identify the lncRNA CALA as a potent regulator of RNA turnover in endothelial cells. We demonstrate that CALA forms cytoplasmic ribonucleoprotein complexes with G3BP1 and regulates endothelial cell functions. A detailed characterization of these G3BP1-positive complexes by mass spectrometry identifies UPF1 and numerous other NMD factors having cytoplasmic G3BP1-association that is CALA-dependent. Importantly, CALA silencing impairs degradation of NMD target transcripts, establishing CALA as a non-coding regulator of RNA steady-state levels in the endothelium.
The lncRNA GATA6-AS epigenetically regulates endothelial gene expression via interaction with LOXL2
(2018)
Neumann, Philipp ; Jaé, Nicolas Christopher ; Knau, Andrea ; Glaser, Simone F. ; Fouani, Youssef ; Rossbach, Oliver ; Krüger, Marcus ; John, David ; Bindereif, Albrecht ; Grote, Phillip ; Boon, Reinier ; Dimmeler, Stefanie
Impaired or excessive growth of endothelial cells contributes to several diseases. However, the functional involvement of regulatory long non-coding RNAs in these processes is not well defined. Here, we show that the long non-coding antisense transcript of GATA6 (GATA6-AS) interacts with the epigenetic regulator LOXL2 to regulate endothelial gene expression via changes in histone methylation. Using RNA deep sequencing, we find that GATA6-AS is upregulated in endothelial cells during hypoxia. Silencing of GATA6-AS diminishes TGF-β2-induced endothelial–mesenchymal transition in vitro and promotes formation of blood vessels in mice. We identify LOXL2, known to remove activating H3K4me3 chromatin marks, as a GATA6-AS-associated protein, and reveal a set of angiogenesis-related genes that are inversely regulated by LOXL2 and GATA6-AS silencing. As GATA6-AS silencing reduces H3K4me3 methylation of two of these genes, periostin and cyclooxygenase-2, we conclude that GATA6-AS acts as negative regulator of nuclear LOXL2 function.
Fouani, Youssef ; Kirchhof, Luisa ; Stanicek, Laura ; Luxán, Guillermo ; Heumüller, Andreas ; Knau, Andrea ; Fischer, Ariane ; Devraj, Kavi ; John, David ; Neumann, Philipp ; Bindereif, Albrecht ; Boon, Reinier ; Liebner, Stefan ; Wittig, Ilka ; Mogler, Carolin ; Karimova, Madina ; Dimmeler, Stefanie ; Jaé, Nicolas Christopher
Vascular integrity is essential for organ homeostasis to prevent edema formation and infiltration of inflammatory cells. Long non-coding RNAs (lncRNAs) are important regulators of gene expression and often expressed in a cell type-specific manner. By screening for endothelial-enriched lncRNAs, we identified the undescribed lncRNA NTRAS to control endothelial cell functions. Silencing of NTRAS induces endothelial cell dysfunction in vitro and increases vascular permeability and lethality in mice. Biochemical analysis revealed that NTRAS, through its CA-dinucleotide repeat motif, sequesters the splicing regulator hnRNPL to control alternative splicing of tight junction protein 1 (TJP1; also named zona occludens 1, ZO-1) pre-mRNA. Deletion of the hnRNPL binding motif in mice (Ntras∆CA/∆CA) significantly repressed TJP1 exon 20 usage, favoring expression of the TJP1α- isoform, which augments permeability of the endothelial monolayer. Ntras∆CA/∆CA mice further showed reduced retinal vessel growth and increased vascular permeability and myocarditis. In summary, this study demonstrates that NTRAS is an essential gatekeeper of vascular integrity.
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