Abstract
The human Hole gene (hHole) encodes a six-transmembrane protein with 319- amino acids. Our previous study showed that hHole was strongly expressed in adult heart and may act as a suppressor of extracellular signal-regulated kinases (ERKs), overactivation of which contributed to pathological cardiac hypertrophy. In this study, it was observed that Hole expression was up-regulated in murine hypertrophic hearts. In a cardiac specific transgenic mouse model, it was observed that overexpression of hHole specifically in heart attenuated cardiac hypertrophy and fibrosis induced by isoproterenol (ISO), with blunted transcriptions of ERK1/2, total ERK1/2 proteins and phosphorylated ERK1/2 (p-ERK1/2) levels. Furthermore, overexpression of hHole in mice by hydrodynamic tail-vein injection with hHole plamids also inhibited cardiac hypertrophy induced by ISO. Our work identified hHole as a novel repressor of cardiac hypertrophy, and provided new insights into the possible target for the prevention or treatment of cardiac diseases.
Keywords: Cardiac hypertrophy, human Hole gene (hHole), isoproterenol (ISO), extracellular signal-regulated kinases (ERKs).
Current Molecular Medicine
Title:Cardiac Specific Overexpression of hHole Attenuates Isoproterenol–Induced Hypertrophic Remodeling through Inhibition of Extracellular Signal-Regulated Kinases (ERKs) Signalling
Volume: 16 Issue: 5
Author(s): X. Ye, Y. Li, X. Wu, X. Mo, X. Fan, S. Luo, G. Dai, X. Wang, F. Chen, Y. Deng, X. Peng, Y. Wan, W. Xu, Z. Jiang, Q. Zeng, L. Cao, Y. Shi, X. Liu, W. Yuan, S. Zhang, X. Zhu, J. Zhou and Y. Wang
Affiliation:
Keywords: Cardiac hypertrophy, human Hole gene (hHole), isoproterenol (ISO), extracellular signal-regulated kinases (ERKs).
Abstract: The human Hole gene (hHole) encodes a six-transmembrane protein with 319- amino acids. Our previous study showed that hHole was strongly expressed in adult heart and may act as a suppressor of extracellular signal-regulated kinases (ERKs), overactivation of which contributed to pathological cardiac hypertrophy. In this study, it was observed that Hole expression was up-regulated in murine hypertrophic hearts. In a cardiac specific transgenic mouse model, it was observed that overexpression of hHole specifically in heart attenuated cardiac hypertrophy and fibrosis induced by isoproterenol (ISO), with blunted transcriptions of ERK1/2, total ERK1/2 proteins and phosphorylated ERK1/2 (p-ERK1/2) levels. Furthermore, overexpression of hHole in mice by hydrodynamic tail-vein injection with hHole plamids also inhibited cardiac hypertrophy induced by ISO. Our work identified hHole as a novel repressor of cardiac hypertrophy, and provided new insights into the possible target for the prevention or treatment of cardiac diseases.
Export Options
About this article
Cite this article as:
Ye X., Li Y., Wu X., Mo X., Fan X., Luo S., Dai G., Wang X., Chen F., Deng Y., Peng X., Wan Y., Xu W., Jiang Z., Zeng Q., Cao L., Shi Y., Liu X., Yuan W., Zhang S., Zhu X., Zhou J. and Wang Y., Cardiac Specific Overexpression of hHole Attenuates Isoproterenol–Induced Hypertrophic Remodeling through Inhibition of Extracellular Signal-Regulated Kinases (ERKs) Signalling, Current Molecular Medicine 2016; 16 (5) . https://dx.doi.org/10.2174/1566524016666160523143704
DOI https://dx.doi.org/10.2174/1566524016666160523143704 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Hydrogels: A Journey from Diapers to Gene Delivery
Mini-Reviews in Medicinal Chemistry Regulatory Mechanisms of Calcineurin Phosphatase Activity
Current Medicinal Chemistry Acute Coronary Syndromes in Patients with Atrial Fibrillation and Heart Failure. Could Novel Oral Anticoagulants be the Solution of the Optimal Antithrombotic Therapy Puzzle?
Cardiovascular & Hematological Agents in Medicinal Chemistry Novel Therapeutic Targets for Phosphodiesterase 5 Inhibitors: current state-of-the-art on systemic arterial hypertension and atherosclerosis
Current Pharmaceutical Biotechnology Potential Treatment of Cardiac Hypertrophy and Heart Failure by Inhibiting the Sarcolemmal Binding of Phospholipase Cβ1b
Current Drug Targets Clinical and Pharmacological Aspects of Immunoprophylaxis for Respiratory Syncytial Virus Infection in High-Risk Infants
Current Drug Metabolism Relaxin Receptors - New Drug Targets for Multiple Disease States
Current Drug Targets New Molecular Targets of Anticancer Therapy – Current Status and Perspectives
Current Medicinal Chemistry Fontan Circulation Might be Associated with Peripartum Cardiomyopathy: A Review of Mechanistic and Clinical Aspects
Current Cardiology Reviews Do Advanced Glycation End Products (AGEs) Contribute to the Comorbidities of Polycystic Ovary Syndrome (PCOS)?
Current Pharmaceutical Design Dynamics of T Cells Repertoire During Trypanosoma cruzi Infection and its Post-Treatment Modulation
Current Medicinal Chemistry Antiviral Drugs that Target Cellular Proteins May Play Major Roles in Combating HIV Resistance
Current Pharmaceutical Design Conditional Cardiac Overexpression of S100A6 Attenuates Myocyte Hypertrophy and Apoptosis Following Myocardial Infarction
Current Pharmaceutical Design Doxorubicin-Loaded Nanoparticles: New Advances in Breast Cancer Therapy
Anti-Cancer Agents in Medicinal Chemistry NAD+, Sirtuins, and Cardiovascular Disease
Current Pharmaceutical Design Adenosine Receptors: What We Know and What We are Learning
Current Topics in Medicinal Chemistry The Heme Oxygenase/Biliverdin Reductase Pathway in Drug Research and Development
Current Drug Metabolism Heart Failure Modulates the Muscle Reflex
Current Cardiology Reviews Restoration of Cardiomyocyte Function in Streptozotocin-Induced Diabetic Rats after Treatment with Vanadate in a Tea Decoction
Current Pharmaceutical Biotechnology Cardiovascular Therapeutics Targets on the NO–sGC–cGMP Signaling Pathway: A Critical Overview
Current Drug Targets