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Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis

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Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis. / Kenneweg, Franziska; Bang, Claudia; Xiao, Ke; Boulanger, Chantal M; Loyer, Xavier; Mazlan, Stephane; Schroen, Blanche; Hermans-Beijnsberger, Steffie; Foinquinos, Ariana; Hirt, Marc N; Eschenhagen, Thomas; Funcke, Sandra; Stojanovic, Stevan; Genschel, Celina; Schimmel, Katharina; Just, Annette; Pfanne, Angelika; Scherf, Kristian; Dehmel, Susann; Raemon-Buettner, Stella M; Fiedler, Jan; Thum, Thomas.

in: MOL THER-NUCL ACIDS, Jahrgang 18, 06.12.2019, S. 363-374.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Kenneweg, F, Bang, C, Xiao, K, Boulanger, CM, Loyer, X, Mazlan, S, Schroen, B, Hermans-Beijnsberger, S, Foinquinos, A, Hirt, MN, Eschenhagen, T, Funcke, S, Stojanovic, S, Genschel, C, Schimmel, K, Just, A, Pfanne, A, Scherf, K, Dehmel, S, Raemon-Buettner, SM, Fiedler, J & Thum, T 2019, 'Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis', MOL THER-NUCL ACIDS, Jg. 18, S. 363-374. https://doi.org/10.1016/j.omtn.2019.09.003

APA

Kenneweg, F., Bang, C., Xiao, K., Boulanger, C. M., Loyer, X., Mazlan, S., Schroen, B., Hermans-Beijnsberger, S., Foinquinos, A., Hirt, M. N., Eschenhagen, T., Funcke, S., Stojanovic, S., Genschel, C., Schimmel, K., Just, A., Pfanne, A., Scherf, K., Dehmel, S., ... Thum, T. (2019). Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis. MOL THER-NUCL ACIDS, 18, 363-374. https://doi.org/10.1016/j.omtn.2019.09.003

Vancouver

Kenneweg F, Bang C, Xiao K, Boulanger CM, Loyer X, Mazlan S et al. Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis. MOL THER-NUCL ACIDS. 2019 Dez 6;18:363-374. https://doi.org/10.1016/j.omtn.2019.09.003

Bibtex

@article{1b5cb41a33644f5fbca3f29e86c8ee83,
title = "Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis",
abstract = "Long non-coding RNAs (lncRNAs) have potential as novel therapeutic targets in cardiovascular diseases, but detailed information about the intercellular lncRNA shuttling mechanisms in the heart is lacking. Here, we report an important novel crosstalk between cardiomyocytes and fibroblasts mediated by the transfer of lncRNA-enriched extracellular vesicles (EVs) in the context of cardiac ischemia. lncRNA profiling identified two hypoxia-sensitive lncRNAs: ENSMUST00000122745 was predominantly found in small EVs, whereas lncRNA Neat1 was enriched in large EVs in vitro and in vivo. Vesicles were taken up by fibroblasts, triggering expression of profibrotic genes. In addition, lncRNA Neat1 was transcriptionally regulated by P53 under basal conditions and by HIF2A during hypoxia. The function of Neat1 was further elucidated in vitro and in vivo. Silencing of Neat1 in vitro revealed that Neat1 was indispensable for fibroblast and cardiomyocyte survival and affected fibroblast functions (reduced migration capacity, stalled cell cycle, and decreased expression of fibrotic genes). Of translational importance, genetic loss of Neat1 in vivo resulted in an impaired heart function after myocardial infarction highlighting its translational relevance.",
author = "Franziska Kenneweg and Claudia Bang and Ke Xiao and Boulanger, {Chantal M} and Xavier Loyer and Stephane Mazlan and Blanche Schroen and Steffie Hermans-Beijnsberger and Ariana Foinquinos and Hirt, {Marc N} and Thomas Eschenhagen and Sandra Funcke and Stevan Stojanovic and Celina Genschel and Katharina Schimmel and Annette Just and Angelika Pfanne and Kristian Scherf and Susann Dehmel and Raemon-Buettner, {Stella M} and Jan Fiedler and Thomas Thum",
note = "Copyright {\textcopyright} 2019 The Author(s). Published by Elsevier Inc. All rights reserved.",
year = "2019",
month = dec,
day = "6",
doi = "10.1016/j.omtn.2019.09.003",
language = "English",
volume = "18",
pages = "363--374",
journal = "MOL THER-NUCL ACIDS",
issn = "2162-2531",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Long Noncoding RNA-Enriched Vesicles Secreted by Hypoxic Cardiomyocytes Drive Cardiac Fibrosis

AU - Kenneweg, Franziska

AU - Bang, Claudia

AU - Xiao, Ke

AU - Boulanger, Chantal M

AU - Loyer, Xavier

AU - Mazlan, Stephane

AU - Schroen, Blanche

AU - Hermans-Beijnsberger, Steffie

AU - Foinquinos, Ariana

AU - Hirt, Marc N

AU - Eschenhagen, Thomas

AU - Funcke, Sandra

AU - Stojanovic, Stevan

AU - Genschel, Celina

AU - Schimmel, Katharina

AU - Just, Annette

AU - Pfanne, Angelika

AU - Scherf, Kristian

AU - Dehmel, Susann

AU - Raemon-Buettner, Stella M

AU - Fiedler, Jan

AU - Thum, Thomas

N1 - Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

PY - 2019/12/6

Y1 - 2019/12/6

N2 - Long non-coding RNAs (lncRNAs) have potential as novel therapeutic targets in cardiovascular diseases, but detailed information about the intercellular lncRNA shuttling mechanisms in the heart is lacking. Here, we report an important novel crosstalk between cardiomyocytes and fibroblasts mediated by the transfer of lncRNA-enriched extracellular vesicles (EVs) in the context of cardiac ischemia. lncRNA profiling identified two hypoxia-sensitive lncRNAs: ENSMUST00000122745 was predominantly found in small EVs, whereas lncRNA Neat1 was enriched in large EVs in vitro and in vivo. Vesicles were taken up by fibroblasts, triggering expression of profibrotic genes. In addition, lncRNA Neat1 was transcriptionally regulated by P53 under basal conditions and by HIF2A during hypoxia. The function of Neat1 was further elucidated in vitro and in vivo. Silencing of Neat1 in vitro revealed that Neat1 was indispensable for fibroblast and cardiomyocyte survival and affected fibroblast functions (reduced migration capacity, stalled cell cycle, and decreased expression of fibrotic genes). Of translational importance, genetic loss of Neat1 in vivo resulted in an impaired heart function after myocardial infarction highlighting its translational relevance.

AB - Long non-coding RNAs (lncRNAs) have potential as novel therapeutic targets in cardiovascular diseases, but detailed information about the intercellular lncRNA shuttling mechanisms in the heart is lacking. Here, we report an important novel crosstalk between cardiomyocytes and fibroblasts mediated by the transfer of lncRNA-enriched extracellular vesicles (EVs) in the context of cardiac ischemia. lncRNA profiling identified two hypoxia-sensitive lncRNAs: ENSMUST00000122745 was predominantly found in small EVs, whereas lncRNA Neat1 was enriched in large EVs in vitro and in vivo. Vesicles were taken up by fibroblasts, triggering expression of profibrotic genes. In addition, lncRNA Neat1 was transcriptionally regulated by P53 under basal conditions and by HIF2A during hypoxia. The function of Neat1 was further elucidated in vitro and in vivo. Silencing of Neat1 in vitro revealed that Neat1 was indispensable for fibroblast and cardiomyocyte survival and affected fibroblast functions (reduced migration capacity, stalled cell cycle, and decreased expression of fibrotic genes). Of translational importance, genetic loss of Neat1 in vivo resulted in an impaired heart function after myocardial infarction highlighting its translational relevance.

U2 - 10.1016/j.omtn.2019.09.003

DO - 10.1016/j.omtn.2019.09.003

M3 - SCORING: Journal article

C2 - 31634682

VL - 18

SP - 363

EP - 374

JO - MOL THER-NUCL ACIDS

JF - MOL THER-NUCL ACIDS

SN - 2162-2531

ER -