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GOLDIC triggers heart failure after MI

DISCOVERIES (ISSN 2359-7232), 2017, October-December issue

CITATION: 

Cordes F, Curaj A, Simsekyilmaz S, Schneider U, Liehn EA. Anti-inflammatory Gold-Induced Autologous Cytokines treatment triggers heart failure after myocardial infarction. Discoveries 2017, 5(4): e80. DOI: 10.15190/d.2017.10

Submitted: December 13th, 2017; Revised: December 31st, 2017; Accepted: December 31st, 2017; Published: December 31st, 2017;

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Anti-inflammatory Gold-Induced Autologous Cytokines treatment triggers heart failure after myocardial infarction

Angus Franziska Cordes (1), Adelina Curaj (1, 2), Sakine Simsekyilmaz (1, 3), Ulrich Schneider (4), Elisa A. Liehn (1, 2, 5, *)

(1) Institute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Germany; 

(2) Victor Babes National Institute of Pathology, Bucharest, Romania; 

(3) Biochemistry Institute, Justus-Liebig-University, Giessen, Germany; 

(4) Arthro Nova Clinic, Ringsee, Germany; 

(5) Human Genetics Laboratory, University of Medicine and Pharmacy, Craiova, Romania;


*Corresponding author: Elisa A. Liehn MD, PhD, Institute for Molecular Cardiovascular Research (IMCAR), University Hospital Aachen, Rheinisch-Westfälische Technische Hochschule Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany; Tel.: +49-241-80 35983; Email: eliehn @ukaachen.de

Abstract

Background: Gold-induced autologous cytokine (GOLDIC) treatment is usually used in the therapy of the inflammatory musculoskeletal disorders (e.g. osteoarthritis in humans) and is able to modulate the inflammatory reaction. Moreover, governed by chemokines and cytokines, the complex inflammatory response after an acute myocardial infarction (MI), the main cause of death worldwide, plays an important role in the preservation of heart function. Therefore, we hypothetized that GOLDIC could also have an important role in ventricular remodeling after MI.

Methods: Myocardial infarction was induced in mice and GOLDIC-enriched serum was injected directly in the infarcted tissue. Four weeks later, the function of the heart, as well as the infarction size and the scar composition was analyzed. Statistical analysis was performed with Prism 6.1 software (GraphPad), using 1-way ANOVA, followed by Newman-Keuls post-hoc-test, as indicated. Data are represented as mean ± SEM. 

Results: Four weeks after MI, GOLDIC-treated mice show significantly decreased heart function and higher infarction size compared to the control group. Immunohistochemistry reveals a significantly increased number of myofibroblasts, correlating with higher collagen content in the infarcted area. Despite impaired heart function, angiogenesis in the GOLDIC-treated group is improved compared with the control, due to the increased vascular endothelial growth factor (VEGF) in the GOLDIC serum. 

Conclusions: In conclusion, GOLDIC treatment impaires the ventricular remodeling, worsening the heart function. Therefore, these systemic effects should be taken into account when new therapies are designed for the musculoskeletal disorders.

Access full text of the manuscript here: 

References

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9. Curaj A, Simsekyilmaz S, Staudt M, Liehn E. Minimal invasive surgical procedure of inducing myocardial infarction in mice. J Vis Exp. 2015; e52197.

10.  Curaj A, Staudt M, Fatu R, Kraaijeveld AO, Jankowski J, et al. Blockade of CCR3 retains the neutrophils, preserving their survival during healing after myocardial infarction. Discoveries 2015; 3: e45.

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