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      Call for Papers: Novel Methods in Vascular and Lymphatic Physiology

      Submit here before June 30, 2025

      About Journal of Vascular Research: 1.8 Impact Factor I 3.4 CiteScore I 0.486 Scimago Journal & Country Rank (SJR)

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      Transcriptional Effects of E3 Ligase Nrdp1 on Hypertrophy in Neonatal Rat Cardiomyocytes by Microarray and Integrated Gene Network Analysis

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          Abstract

          Objective: Neuregulin receptor degradation protein-1 (Nrdp1) is a novel E3 ubiquitin ligase, and we have previously shown that overexpression of Nrdp1 increased cardiomyocyte injury. However, the role of Nrdp1 in myocardial hypertrophy is unclear. In the present study, we clarified the molecular mechanisms of angiotensin II (Ang II)-induced cardiomyocyte hypertrophy regulated by Nrdp1 based on genome-wide transcriptional analysis. Methods: Neonatal rat cardiomyocytes were infected with adenoviruses containing green fluorescent protein (Ad-GFP) or wild-type Nrdp1 (Ad-Nrdp1), and then treated with Ang II for 36 h. Detection of differentially expressed genes was achieved with an Affymetrix Rat Gene 2.0 Array and Cluster and Java TreeView software. Results and Conclusion: Microarray data analysis demonstrated that Nrdp1 overexpression affected the expression of 12,140 mRNA genes in Ang II-induced cardiomyocyte hypertrophy, including the upregulation of 12,044 and the downregulation of 96. Gene ontology and globe signal transduction network analysis showed that Nrdp1 affected the expression of many genes related to stimulus response, the cell receptor pathway, and cell growth. Pathway network analysis identified myocardial metabolism, DNA replication, and the cell cycle as the most important pathways targeted by Nrdp1. lncRNA-mRNA coexpression network analysis showed that two core lncRNAs, NONRATT057160 and NONRATT054243, were involved in cardiomyotrophy regulated by Nrdp1 in cardiomyocytes. Taken together, these data provide compelling clues for further exploration of the function of Nrdp1 in heart disease.

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          The E3 ubiquitin ligase Nrdp1 'preferentially' promotes TLR-mediated production of type I interferon.

          Mingjin Yang, Xiongfei Xu, Nan Li … (2009)
          E3 ubiquitin ligases are important in both innate and adaptive immunity. Here we report that Nrdp1, an E3 ubiquitin ligase, inhibited the production of proinflammatory cytokines but increased interferon-beta production in Toll-like receptor-triggered macrophages by suppressing adaptor MyD88-dependent activation of transcription factors NF-kappaB and AP-1 while promoting activation of the kinase TBK1 and transcription factor IRF3. Nrdp1 directly bound and polyubiquitinated MyD88 and TBK1, which led to degradation of MyD88 and activation of TBK1. Knockdown of Nrdp1 inhibited the degradation of MyD88 and the activation of TBK1 and IRF3. Nrdp1-transgenic mice showed resistance to lipopolysaccharide-induced endotoxin shock and to infection with vesicular stomatitis virus. Our data suggest that Nrdp1 functions as both an adaptor protein and an E3 unbiquitin ligase to regulate TLR responses in different ways.
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            The diabetes susceptibility gene Clec16a regulates mitophagy.

            Scott A. Soleimanpour, Aditi Gupta, Marina Bakay … (2014)
            Clec16a has been identified as a disease susceptibility gene for type 1 diabetes, multiple sclerosis, and adrenal dysfunction, but its function is unknown. Here we report that Clec16a is a membrane-associated endosomal protein that interacts with E3 ubiquitin ligase Nrdp1. Loss of Clec16a leads to an increase in the Nrdp1 target Parkin, a master regulator of mitophagy. Islets from mice with pancreas-specific deletion of Clec16a have abnormal mitochondria with reduced oxygen consumption and ATP concentration, both of which are required for normal β cell function. Indeed, pancreatic Clec16a is required for normal glucose-stimulated insulin release. Moreover, patients harboring a diabetogenic SNP in the Clec16a gene have reduced islet Clec16a expression and reduced insulin secretion. Thus, Clec16a controls β cell function and prevents diabetes by controlling mitophagy. This pathway could be targeted for prevention and control of diabetes and may extend to the pathogenesis of other Clec16a- and Parkin-associated diseases. Copyright © 2014 Elsevier Inc. All rights reserved.
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              Sphingosine-1-Phosphate Receptor Agonist Fingolimod Increases Myocardial Salvage and Decreases Adverse Postinfarction Left Ventricular Remodeling in a Porcine Model of Ischemia/Reperfusion.

              Carlos G. Santos-Gallego, Torsten P Vahl, Georg Goliasch … (2016)
              Fingolimod, a sphingosine-1-phosphate receptor agonist, is used for the treatment of multiple sclerosis and exerts antiapoptotic properties. We hypothesized that sphingosine-1-phosphate receptor activation with fingolimod during acute myocardial infarction (MI) inhibits apoptosis, leading to increased myocardial salvage, reduced infarct size, and mitigated left ventricular (LV) remodeling in a porcine model of ischemia/reperfusion.
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                Author and article information

                Journal
                Journal ID (publisher-id): CRD
                Journal ID (nlm-ta): Cardiology
                Journal ID (doi): 10.1159/issn.0008-6312
                Title: Cardiology
                Publisher: S. Karger AG
                ISSN (Print): 0008-6312
                ISSN (Electronic): 1421-9751
                Publication date Subscription-year: 2016
                Publication date (Print): November 2016
                Publication date (Electronic): 19 July 2016
                Volume: 135
                Issue: 4
                Pages: 203-215
                Affiliations
                aDepartment of Pathophysiology, Institute of Basic Medical and Forensic Science, Baotou Medical College, and bDepartment of Neurosurgery, First Affiliated Hospital of Baotou Medical College, Baotou, and cThe Central Laboratory, Shenzhen Second People's Hospital, Shenzhen University First Affiliated Hospital, Shenzhen, China
                Author notes
                *Yuan Zhang, MD, PhD, Department of Pathophysiology, Institute of Basic Medical and Forensic Science, Baotou Medical College, No. 31, Jianshe Road, Donghe District, Baotou 014060 (China), E-Mail susanyuan821@163.com
                Article
                Publisher ID: 447235 Other ID: Cardiology 2016;135:203-215
                DOI: 10.1159/000447235
                PubMed ID: 27428330
                SO-VID: a14053bb-ab42-4f9e-9914-56e0a9107d41
                Copyright © © 2016 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Date received : 08 April 2016
                Date accepted : 26 May 2016
                Page count
                Figures: 6, Tables: 2, References: 38, Pages: 13
                Categories
                Subject: Original Research

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: Cardiomyocyte hypertrophy,Angiotensin II,E3 ubiquitin ligase,Microarray,Neuregulin receptor degradation protein-1
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: Cardiomyocyte hypertrophy, Angiotensin II, E3 ubiquitin ligase, Microarray, Neuregulin receptor degradation protein-1

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