LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 7 of total 7

Search options

  1. Article ; Online: The lncRNA Sweetheart regulates compensatory cardiac hypertrophy after myocardial injury in murine males.

    Rogala, Sandra / Ali, Tamer / Melissari, Maria-Theodora / Währisch, Sandra / Schuster, Peggy / Sarre, Alexandre / Emídio, Rebeca Cordellini / Boettger, Thomas / Rogg, Eva-Maria / Kaur, Jaskiran / Krishnan, Jaya / Dumbović, Gabrijela / Dimmeler, Stefanie / Ounzain, Samir / Pedrazzini, Thierry / Herrmann, Bernhard G / Grote, Phillip

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 7024

    Abstract: After myocardial infarction in the adult heart the remaining, non-infarcted tissue adapts to compensate the loss of functional tissue. This adaptation requires changes in gene expression networks, which are mostly controlled by transcription regulating ... ...

    Abstract After myocardial infarction in the adult heart the remaining, non-infarcted tissue adapts to compensate the loss of functional tissue. This adaptation requires changes in gene expression networks, which are mostly controlled by transcription regulating proteins. Long non-coding transcripts (lncRNAs) are taking part in fine-tuning such gene programs. We describe and characterize the cardiomyocyte specific lncRNA Sweetheart RNA (Swhtr), an approximately 10 kb long transcript divergently expressed from the cardiac core transcription factor coding gene Nkx2-5. We show that Swhtr is dispensable for normal heart development and function but becomes essential for the tissue adaptation process after myocardial infarction in murine males. Re-expressing Swhtr from an exogenous locus rescues the Swhtr null phenotype. Genes that depend on Swhtr after cardiac stress are significantly occupied and therefore most likely regulated by NKX2-5. The Swhtr transcript interacts with NKX2-5 and disperses upon hypoxic stress in cardiomyocytes, indicating an auxiliary role of Swhtr for NKX2-5 function in tissue adaptation after myocardial injury.
    MeSH term(s) Male ; Mice ; Animals ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Myocytes, Cardiac/metabolism ; Cardiomegaly/genetics ; Cardiomegaly/metabolism ; Myocardial Infarction/metabolism ; Heart Injuries
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2023-11-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-42760-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: The lncRNA Locus Handsdown Regulates Cardiac Gene Programs and Is Essential for Early Mouse Development.

    Ritter, Nicole / Ali, Tamer / Kopitchinski, Nina / Schuster, Peggy / Beisaw, Arica / Hendrix, David A / Schulz, Marcel H / Müller-McNicoll, Michaela / Dimmeler, Stefanie / Grote, Phillip

    Developmental cell

    2019  Volume 50, Issue 5, Page(s) 644–657.e8

    Abstract: Precisely controlled gene regulatory networks are required during embryonic development to give rise to various structures, including those of the cardiovascular system. Long non-coding RNA (lncRNA) loci are known to be important regulators of these ... ...

    Abstract Precisely controlled gene regulatory networks are required during embryonic development to give rise to various structures, including those of the cardiovascular system. Long non-coding RNA (lncRNA) loci are known to be important regulators of these genetic programs. We have identified a novel and essential lncRNA locus Handsdown (Hdn), active in early heart cells, and show by genetic inactivation that it is essential for murine development. Hdn displays haploinsufficiency for cardiac development as Hdn-heterozygous adult mice exhibit hyperplasia in the right ventricular wall. Transcriptional activity of the Hdn locus, independent of its RNA, suppresses its neighboring gene Hand2. We reveal a switch in a topologically associated domain in differentiation of the cardiac lineage, allowing the Hdn locus to directly interact with regulatory elements of the Hand2 locus.
    MeSH term(s) Animals ; Cell Differentiation ; Cells, Cultured ; Gene Expression Regulation, Developmental ; Haploinsufficiency ; Heart/embryology ; Mice ; Mice, Inbred C57BL ; Mouse Embryonic Stem Cells/cytology ; Mouse Embryonic Stem Cells/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2019-08-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2019.07.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5742: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 76: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Erratum to: Endogenous developmental endothelial locus-1 limits ischaemia-related angiogenesis by blocking inflammation.

    Klotzsche-von Ameln, Anne / Cremer, Sebastian / Hoffmann, Jedrzej / Schuster, Peggy / Khedr, Sherif / Korovina, Irina / Troullinaki, Maria / Neuwirth, Ales / Sprott, David / Chatzigeorgiou, Antonios / Economopoulou, Matina / Orlandi, Alessia / Hain, Andreas / Zeiher, Andreas M / Deussen, Andreas / Hajishengallis, George / Dimmeler, Stefanie / Chavakis, Triantafyllos / Chavakis, Emmanouil

    Thrombosis and haemostasis

    2019  Volume 117, Issue 6, Page(s) e1

    Language English
    Publishing date 2019-12-16
    Publishing country Germany
    Document type Journal Article ; Published Erratum
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1055/s-0039-1696711
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.192: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 433: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: Endogenous developmental endothelial locus-1 limits ischaemia-related angiogenesis by blocking inflammation.

    Klotzsche-von Ameln, Anne / Cremer, Sebastian / Hoffmann, Jedrzej / Schuster, Peggy / Khedr, Sherif / Korovina, Irina / Troullinaki, Maria / Neuwirth, Ales / Sprott, David / Chatzigeorgiou, Antonios / Economopoulou, Matina / Orlandi, Alessia / Hain, Andreas / Zeiher, Andreas M / Deussen, Andreas / Hajishengallis, George / Dimmeler, Stefanie / Chavakis, Triantafyllos / Chavakis, Emmanouil

    Thrombosis and haemostasis

    2017  Volume 117, Issue 6, Page(s) 1150–1163

    Abstract: We have recently identified endothelial cell-secreted developmental endothelial locus-1 (Del-1) as an endogenous inhibitor of β2-integrin-dependent leukocyte infiltration. Del-1 was previously also implicated in angiogenesis. Here, we addressed the role ... ...

    Abstract We have recently identified endothelial cell-secreted developmental endothelial locus-1 (Del-1) as an endogenous inhibitor of β2-integrin-dependent leukocyte infiltration. Del-1 was previously also implicated in angiogenesis. Here, we addressed the role of endogenously produced Del-1 in ischaemia-related angiogenesis. Intriguingly, Del-1-deficient mice displayed increased neovascularisation in two independent ischaemic models (retinopathy of prematurity and hind-limb ischaemia), as compared to Del-1-proficient mice. On the contrary, angiogenic sprouting in vitro or ex vivo (aortic ring assay) and physiological developmental retina angiogenesis were not affected by Del-1 deficiency. Mechanistically, the enhanced ischaemic neovascularisation in Del-1-deficiency was linked to higher infiltration of the ischaemic tissue by CD45+ haematopoietic and immune cells. Moreover, Del-1-deficiency promoted β2-integrin-dependent adhesion of haematopoietic cells to endothelial cells in vitro, and the homing of hematopoietic progenitor cells and of immune cell populations to ischaemic muscles in vivo. Consistently, the increased hind limb ischaemia-related angiogenesis in Del-1 deficiency was completely reversed in mice lacking both Del-1 and the β2-integrin LFA-1. Additionally, enhanced retinopathy-associated neovascularisation in Del-1-deficient mice was reversed by LFA-1 blockade. Our data reveal a hitherto unrecognised function of endogenous Del-1 as a local inhibitor of ischaemia-induced angiogenesis by restraining LFA-1-dependent homing of pro-angiogenic haematopoietic cells to ischaemic tissues. Our findings are relevant for the optimisation of therapeutic approaches in the context of ischaemic diseases.
    MeSH term(s) Animals ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cell Adhesion ; Cell Movement ; Disease Models, Animal ; Endothelium, Vascular/physiology ; Extremities/pathology ; Hematopoietic Stem Cells/physiology ; Human Umbilical Vein Endothelial Cells ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Intercellular Signaling Peptides and Proteins ; Ischemia/immunology ; Ischemia/metabolism ; Leukocytes/physiology ; Lymphocyte Function-Associated Antigen-1/genetics ; Lymphocyte Function-Associated Antigen-1/immunology ; Lymphocyte Function-Associated Antigen-1/metabolism ; Mice ; Mice, Knockout ; Neovascularization, Physiologic ; RNA, Small Interfering/genetics ; Retinopathy of Prematurity/immunology ; Retinopathy of Prematurity/metabolism
    Chemical Substances Carrier Proteins ; EDIL3 protein, human ; Edil3 protein, mouse ; Intercellular Signaling Peptides and Proteins ; Lymphocyte Function-Associated Antigen-1 ; RNA, Small Interfering
    Language English
    Publishing date 2017-04-27
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1160/TH16-05-0354
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.192: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 433: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article: Endogenous developmental endothelial locus-1 limits ischaemia- related angiogenesis by blocking inflammation

    Klotzsche - von Ameln, Anne / Cremer, Sebastian / Hoffmann, Jedrzej / Schuster, Peggy / Khedr, Sherif / Korovina, Irina / Troullinaki, Maria / Neuwirth, Ales / Sprott, David / Chatzigeorgiou, Antonios / Economopoulou, Matina / Orlandi, Alessia / Hain, Andreas / Zeiher, Andreas M. / Deussen, Andreas / Hajishengallis, George / Dimmeler, Stefanie / Chavakis, Triantafyllos / Chavakis, Emmanouil

    Thrombosis and Haemostasis

    2017  Volume 56, Issue 06, Page(s) 1150–1163

    Abstract: We have recently identified endothelial cell-secreted developmental endothelial locus-1 (Del-1) as an endogenous inhibitor of β2-integrin–dependent leukocyte infiltration. Del-1 was previously also implicated in angiogenesis. Here, we addressed the role ... ...

    Abstract We have recently identified endothelial cell-secreted developmental endothelial locus-1 (Del-1) as an endogenous inhibitor of β2-integrin–dependent leukocyte infiltration. Del-1 was previously also implicated in angiogenesis. Here, we addressed the role of endogenously produced Del-1 in ischaemia-related angiogenesis. Intriguingly, Del-1–deficient mice displayed increased neovascularisation in two independent ischaemic models (retinopathy of prematurity and hind-limb ischaemia), as compared to Del-1–proficient mice. On the contrary, angiogenic sprouting in vitro or ex vivo (aortic ring assay) and physiological developmental retina angiogenesis were not affected by Del-1 deficiency. Mechanistically, the enhanced ischaemic neovascularisation in Del-1-deficiency was linked to higher infiltration of the ischaemic tissue by CD45+ haematopoietic and immune cells. Moreover, Del-1-deficiency promoted β2-integrin–dependent adhesion of haematopoietic cells to endothelial cells in vitro, and the homing of hematopoietic progenitor cells and of immune cell populations to ischaemic muscles in vivo. Consistently, the increased hind limb ischaemia-related angiogenesis in Del-1 deficiency was completely reversed in mice lacking both Del-1 and the β2-integrin LFA-1. Additionally, enhanced retinopathy-associated neovascularisation in Del-1-deficient mice was reversed by LFA-1 blockade. Our data reveal a hitherto unrecognised function of endogenous Del-1 as a local inhibitor of ischaemia-induced angiogenesis by restraining LFA-1–dependent homing of pro-angiogenic haematopoietic cells to ischaemic tissues. Our findings are relevant for the optimisation of therapeutic approaches in the context of ischaemic diseases. Supplementary Material to this article is available online at www.thrombosis-online.com.
    Keywords Angiogenesis ; integrins ; leukocytes
    Language English
    Publishing date 2017-01-01
    Publisher Schattauer GmbH
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1160/TH16-05-0354
    Database Thieme publisher's database

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.192: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 433: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article: Erratum to: Endogenous developmental endothelial locus-1 limits ischaemia-related angiogenesis by blocking inflammation

    Klotzsche-von Ameln, Anne / Cremer, Sebastian / Hoffmann, Jedrzej / Schuster, Peggy / Khedr, Sherif / Korovina, Irina / Troullinaki, Maria / Neuwirth, Ales / Sprott, David / Chatzigeorgiou, Antonios / Economopoulou, Matina / Orlandi, Alessia / Hain, Andreas / Zeiher, Andreas M. / Deussen, Andreas / Hajishengallis, George / Dimmeler, Stefanie / Chavakis, Triantafyllos / Chavakis, Emmanouil

    Thrombosis and Haemostasis

    2017  Volume 117, Issue 06, Page(s) e1–e1

    Language English
    Publishing date 2017-06-01
    Publisher Georg Thieme Verlag KG
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1055/s-0039-1696711
    Database Thieme publisher's database

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.192: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 433: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  7. Article ; Online: Rare Variants in BNC2 Are Implicated in Autosomal-Dominant Congenital Lower Urinary-Tract Obstruction.

    Kolvenbach, Caroline M / Dworschak, Gabriel C / Frese, Sandra / Japp, Anna S / Schuster, Peggy / Wenzlitschke, Nina / Yilmaz, Öznur / Lopes, Filipa M / Pryalukhin, Alexey / Schierbaum, Luca / van der Zanden, Loes F M / Kause, Franziska / Schneider, Ronen / Taranta-Janusz, Katarzyna / Szczepańska, Maria / Pawlaczyk, Krzysztof / Newman, William G / Beaman, Glenda M / Stuart, Helen M /
    Cervellione, Raimondo M / Feitz, Wouter F J / van Rooij, Iris A L M / Schreuder, Michiel F / Steffens, Martijn / Weber, Stefanie / Merz, Waltraut M / Feldkötter, Markus / Hoppe, Bernd / Thiele, Holger / Altmüller, Janine / Berg, Christoph / Kristiansen, Glen / Ludwig, Michael / Reutter, Heiko / Woolf, Adrian S / Hildebrandt, Friedhelm / Grote, Phillip / Zaniew, Marcin / Odermatt, Benjamin / Hilger, Alina C

    American journal of human genetics

    2019  Volume 104, Issue 5, Page(s) 994–1006

    Abstract: Congenital lower urinary-tract obstruction (LUTO) is caused by anatomical blockage of the bladder outflow tract or by functional impairment of urinary voiding. About three out of 10,000 pregnancies are affected. Although several monogenic causes of ... ...

    Abstract Congenital lower urinary-tract obstruction (LUTO) is caused by anatomical blockage of the bladder outflow tract or by functional impairment of urinary voiding. About three out of 10,000 pregnancies are affected. Although several monogenic causes of functional obstruction have been defined, it is unknown whether congenital LUTO caused by anatomical blockage has a monogenic cause. Exome sequencing in a family with four affected individuals with anatomical blockage of the urethra identified a rare nonsense variant (c.2557C>T [p.Arg853
    MeSH term(s) Adult ; Animals ; Child ; Chromosome Aberrations ; DNA-Binding Proteins/genetics ; Female ; Fetal Diseases/genetics ; Fetal Diseases/pathology ; Genes, Dominant ; Gestational Age ; Humans ; Male ; Mice ; Middle Aged ; Mutation ; Pedigree ; Pregnancy ; Urinary Bladder Neck Obstruction/congenital ; Urinary Bladder Neck Obstruction/genetics ; Urinary Bladder Neck Obstruction/pathology ; Zebrafish
    Chemical Substances BNC2 protein, human ; DNA-Binding Proteins
    Language English
    Publishing date 2019-05-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 219384-x
    ISSN 1537-6605 ; 0002-9297
    ISSN (online) 1537-6605
    ISSN 0002-9297
    DOI 10.1016/j.ajhg.2019.03.023
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 107: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top