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Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis.
Nat Commun 2019; 10(1):4317NC

Abstract

Circular RNAs are generated from many protein-coding genes, but their role in cardiovascular health and disease states remains unknown. Here we report identification of circRNA transcripts that are differentially expressed in post myocardial infarction (MI) mouse hearts including circFndc3b which is significantly down-regulated in the post-MI hearts. Notably, the human circFndc3b ortholog is also significantly down-regulated in cardiac tissues of ischemic cardiomyopathy patients. Overexpression of circFndc3b in cardiac endothelial cells increases vascular endothelial growth factor-A expression and enhances their angiogenic activity and reduces cardiomyocytes and endothelial cell apoptosis. Adeno-associated virus 9 -mediated cardiac overexpression of circFndc3b in post-MI hearts reduces cardiomyocyte apoptosis, enhances neovascularization and improves left ventricular functions. Mechanistically, circFndc3b interacts with the RNA binding protein Fused in Sarcoma to regulate VEGF expression and signaling. These findings highlight a physiological role for circRNAs in cardiac repair and indicate that modulation of circFndc3b expression may represent a potential strategy to promote cardiac function and remodeling after MI.

Authors+Show Affiliations

Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Division of Cardiovascular Diseases, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, 35294, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Department of Biochemistry and Biophysics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Department of Biomedical Sciences, University of Missouri, Columbia, MO, 65211, USA.Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, 44195, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Department of Biochemistry and Biophysics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, 19104, USA.Zena & Michael A. Weiner Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.Cardiovascular Research Center and Department of Physiology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA. Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA. raj.kishore@temple.edu. Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA. raj.kishore@temple.edu.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31541092

Citation

Garikipati, Venkata Naga Srikanth, et al. "Circular RNA CircFndc3b Modulates Cardiac Repair After Myocardial Infarction Via FUS/VEGF-A Axis." Nature Communications, vol. 10, no. 1, 2019, p. 4317.
Garikipati VNS, Verma SK, Cheng Z, et al. Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis. Nat Commun. 2019;10(1):4317.
Garikipati, V. N. S., Verma, S. K., Cheng, Z., Liang, D., Truongcao, M. M., Cimini, M., ... Kishore, R. (2019). Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis. Nature Communications, 10(1), p. 4317. doi:10.1038/s41467-019-11777-7.
Garikipati VNS, et al. Circular RNA CircFndc3b Modulates Cardiac Repair After Myocardial Infarction Via FUS/VEGF-A Axis. Nat Commun. 2019 Sep 20;10(1):4317. PubMed PMID: 31541092.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis. AU - Garikipati,Venkata Naga Srikanth, AU - Verma,Suresh Kumar, AU - Cheng,Zhongjian, AU - Liang,Dongming, AU - Truongcao,May M, AU - Cimini,Maria, AU - Yue,Yujia, AU - Huang,Grace, AU - Wang,Chunlin, AU - Benedict,Cindy, AU - Tang,Yan, AU - Mallaredy,Vandana, AU - Ibetti,Jessica, AU - Grisanti,Laurel, AU - Schumacher,Sarah M, AU - Gao,Erhe, AU - Rajan,Sudarsan, AU - Wilusz,Jeremy E, AU - Goukassian,David, AU - Houser,Steven R, AU - Koch,Walter J, AU - Kishore,Raj, Y1 - 2019/09/20/ PY - 2018/08/05/received PY - 2019/07/30/accepted PY - 2019/9/22/entrez PY - 2019/9/22/pubmed PY - 2019/9/22/medline SP - 4317 EP - 4317 JF - Nature communications JO - Nat Commun VL - 10 IS - 1 N2 - Circular RNAs are generated from many protein-coding genes, but their role in cardiovascular health and disease states remains unknown. Here we report identification of circRNA transcripts that are differentially expressed in post myocardial infarction (MI) mouse hearts including circFndc3b which is significantly down-regulated in the post-MI hearts. Notably, the human circFndc3b ortholog is also significantly down-regulated in cardiac tissues of ischemic cardiomyopathy patients. Overexpression of circFndc3b in cardiac endothelial cells increases vascular endothelial growth factor-A expression and enhances their angiogenic activity and reduces cardiomyocytes and endothelial cell apoptosis. Adeno-associated virus 9 -mediated cardiac overexpression of circFndc3b in post-MI hearts reduces cardiomyocyte apoptosis, enhances neovascularization and improves left ventricular functions. Mechanistically, circFndc3b interacts with the RNA binding protein Fused in Sarcoma to regulate VEGF expression and signaling. These findings highlight a physiological role for circRNAs in cardiac repair and indicate that modulation of circFndc3b expression may represent a potential strategy to promote cardiac function and remodeling after MI. SN - 2041-1723 UR - https://www.unboundmedicine.com/medline/citation/31541092/Circular_RNA_CircFndc3b_modulates_cardiac_repair_after_myocardial_infarction_via_FUS/VEGF-A_axis L2 - http://dx.doi.org/10.1038/s41467-019-11777-7 DB - PRIME DP - Unbound Medicine ER -