Basic Study
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Cardiol. Aug 26, 2017; 9(8): 673-684
Published online Aug 26, 2017. doi: 10.4330/wjc.v9.i8.673
Interleukin-19 is cardioprotective in dominant negative cyclic adenosine monophosphate response-element binding protein-mediated heart failure in a sex-specific manner
Danielle R Bruns, Alexander R Ghincea, Christian V Ghincea, Yasu-Taka Azuma, Peter A Watson, Michael V Autieri, Lori A Walker
Danielle R Bruns, Alexander R Ghincea, Christian V Ghincea, Lori A Walker, Division of Cardiology, Department of Medicine, University of Colorado-Denver, Aurora, CO 80045, United States
Yasu-Taka Azuma, Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University Graduate School of Life and Environmental Science, Osaka 599-8351, Japan
Peter A Watson, Department of Medicine and Endocrinology, University of Colorado-Denver, Aurora, CO 80045, United States
Peter A Watson, Denver Veterans Affairs Medical Center, Denver, CO 80220, United States
Michael V Autieri, Independence Blue Cross Cardiovascular Research Center, Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19122, United States
Author contributions: Bruns DR was involved in conception and design of research, collected, analyzed, and interpreted data, and drafted the manuscript; Ghincea AR and Ghincea CV collected data; Azuma YT approved the final manuscript; Watson PA was involved in conception and design of research; Autieri MV contributed to intellectual design of research, edited and revised final manuscript; Walker LA was involved in conception and design of research, interpretation of data, editing, revising, and approval of final manuscript.
Supported by The University of Colorado-Denver Center for Women’s Health Research (to Walker LA); NIH NHLBI HL007822-19 (to Bruns DR); NIH NHLBI HL117724 (to Autieri MV); NIH NHLBI HL115575 (to Autieri MV).
Institutional review board statement: Human subjects research is governed by the Colorado Multiple Institutional Review Board (COMIRB # IORG0000433). However, no human subjects were included in this research.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee at the University of Colorado-Denver [Protocol # B-78616(05)1D].
Conflict-of-interest statement: The authors declare that they have no competing interests.
Data sharing statement: Complete dataset and statistical analyses available from the corresponding author at lori.walker@ucdenver.edu.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Lori A Walker, PhD, Division of Cardiology, Department of Medicine, University of Colorado-Denver, 12700 E. 19th Ave, Aurora, CO 80045, United States. lori.walker@ucdenver.edu
Telephone: +1-303-7245420
Received: January 11, 2017
Peer-review started: January 16, 2017
First decision: April 17, 2017
Revised: July 19, 2017
Accepted: July 21, 2017
Article in press: July 24, 2017
Published online: August 26, 2017
Core Tip

Core tip: Heart failure (HF) is a sexually dimorphic disease. In a female-dominant model of HF, the do-minant negative cyclic AMP response-element binding protein (dnCREB) mouse, female mice show accelerated cardiac morbidity and mortality alongside downregulated interleukin-19 (IL-19) expression, while male mice maintain IL-19 expression and are protected against cardiac dysfunction. We generated a novel double transgenic mouse with dnCREB and IL-19 knockout to test the hypothesis that IL-19 is cardioprotective. We show accelerated cardiac morbidity only in male mice, supporting the hypothesis that IL-19 is a sex-specific cardioprotective cytokine.