News & Events

The German Society for Cardiology (DGK) - Heart and Circulatory Research e.V. promotes the next generation of scientists in cardiology and cardiovascular basic subjects by awarding DGK research grants. 

Dr. Mohammed Rabiul Hosen, a member of the TRR259, has now received such a research grant of € 50,000 for his research project for 2021.

Dr. Hosen together with his team involved in research on cardiovascular disease (CVD), from investigating the underlying molecular mechanisms of pathogenesis in coronary heart diseases (CHDs) to the development of holistic RNA-based therapeutic approaches for the diagnosis ("Liquid Biopsies") and treatment of multifactorial CVDs. Since his PhD research at the Inst. of Cardiovascular Regeneration, Goethe University Frankfurt, he has been working on the development of RNA-based cardiovascular biomarkers/therapies by focusing on different CVDs, including atherosclerosis and its sequelae, and implementing in vitro and in vivo models (myocardial infarction, atherosclerosis, aortic valve stenosis, and heart failure).

Congratulations and good luck with your work.

MicroRNA-mediated vascular intercellular communication is altered in chronic kidney disease

Chronic kidney disease (CKD) is an independent risk factor for the development of coronary artery disease (CAD). For both, CKD and CAD, the intercellular transfer of microRNAs (miR) through extracellular vesicles (EVs) is an important factor of disease development. Whether the combination of CAD and CKD affects endothelial function through cellular crosstalk of EV-incorporated miRs is still unknown.
The group of Andreas Zietzer et. al. could shown in this paper that EV-miR-mediated vascular intercellular communication is altered in patients with CAD and CKD, promoting CKD-induced endothelial dysfunction.

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The "Young Investigator Awards" are presented every year at the annual conference of the German Cardiac Society (DGK). Young scientists who are not older than 35 years are honored. Several young cardiologists from the heart center of the University Hospital were honored this year also a member of the TRR259: The TRR259 member Dr. Sven Thomas Niepmann was awarded with the first prize (1.500€) for his work: “Cyclodextrin reduces aortic valve stenosis development in mice”

Link to the DGK-Website

Pulmonary hypertension associated with left-sided heart failure

Pulmonary hypertension is a common phenomenon in heart failure patients that is highly relevant for morbidity and outcome. Although postcapillary in nature, the pathophysiology of pulmonary hypertension in patients with heart failure with reduced or preserved ejection fraction is complex, and decisions about management strategies remain challenging.

Recently, the hemodynamic definitions and subclassification of postcapillary pulmonary hypertension have been revisited. The distinction between isolated postcapillary pulmonary hypertension (IpcPH) and combined post and precapillary pulmonary hypertension (CpcPH) and their definition are essential. Novel data on the prognostic impact of hemodynamic variables and right ventricular function highlight the importance of cardiopulmonary interaction in patients with left-sided heart failure (LHF). Furthermore, the impact of management strategies including medical therapy, remote hemodynamic monitoring, and interventional approaches on hemodynamics and outcome has recently been investigated. Here, the group of Joana Adler et. al critically review recent developments and future considerations in this field, and highlight distinct treatment strategies targeting the underlying left heart condition, the pulmonary circulation, and/or impaired right ventricular function.

Nitro-fatty acids suppress ischemic ventricular arrhythmias by preserving calcium homeostasis

Nitro-fatty acids are electrophilic anti-inflammatory mediators which are generated during myocardial ischemic injury. Whether these species exert anti-arrhythmic effects in the acute phase of myocardial ischemia has not been investigated so far. The group of Martin Mollenhauer et. al demonstrate that pretreatment of mice with 9- and 10-nitro-octadec-9-enoic acid (nitro-oleic acid, NO2-OA) significantly reduced the susceptibility to develop acute ventricular tachycardia (VT). Accordingly, epicardial mapping revealed a markedly enhanced homogeneity in ventricular conduction. NO2-OA treatment of isolated cardiomyocytes lowered the number of spontaneous contractions upon adrenergic isoproterenol stimulation and nearly abolished ryanodine receptor type 2 (RyR2)-dependent sarcoplasmic Ca2+ leak. NO2-OA also significantly reduced RyR2-phosphorylation by inhibition of increased CaMKII activity. Thus, NO2-OA might be a novel pharmacological option for the prevention of VT development.

 NO₂-OA prevents acute ischemia induced ventricular tachycardias.

The RNA-binding protein hnRNPU regulates the sorting of microRNA-30c-5p into large extracellular vesicles

The transfer of microRNAs (miRs) via extracellular vesicles (EVs) is a functionally relevant mechanism of intercellular communication that regulates both organ homoeostasis and disease development. Little is known about the packaging of miRs into EVs. Previous studies have shown that certain miRs are exported by RNA-binding proteins into small EVs, while for other miRs and for large EVs, in general, the export mechanisms remain unclear. Therefore, a proteomic analysis of endothelial cell-derived large EVs was performed, which revealed that heterogeneous nuclear ribonucleoprotein U (hnRNPU) is abundantly present in EVs. The specific role of hnRNPU for vesicular miR-sorting was confirmed independently by gain- and loss-of-function experiments.

In summary the group of Felix Jansen (AG Jansen), Zietzer and Hosen et. al. could show that hnRNPU retains miR-30c-5p and other miRs and thereby prevents their export into large EVs. The data presented provide a novel and functionally relevant mechanism of vesicular miR export.

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 Graphical summary of the study results (https://www.tandfonline.com/doi/full/10.1080/20013078.2020.1786967)

Adenosine/A2B Receptor Signaling Ameliorates the Effects of Aging and Counteracts Obesity

Increasing abdominal girth and shrinking muscles are two common side effects of aging. Researchers at the University of Bonn have discovered a receptor in mice that regulates both effects. Experiments with human cell cultures suggest that the corresponding signaling pathways might also exist in humans. The study, which also involved researchers from Spain, Finland, Belgium, Denmark and the USA, has now been published in the renowned journal "Cell Metabolism"

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MicroRNAs As Master Regulators of Atherosclerosis: From Pathogenesis to Novel Therapeutic Options

The Department of Internal Medicine II from the University Bonn published a new paper about microRNAs (miRNAs) as master regulators of atherosclerosis. Cardiovascular disease remains the major cause of morbidity and mortality worldwide. There are indications that atherosclerosis and its sequelae, coronary artery disease, contribute to the majority of cardiovascular death. It was shown that small RNAs, especially micro RNAs (miRNAs) are dynamic regulators of disease pathogenesis. They are considered to be central during the regulation of gene expression through numerous mechanisms and provide a means to develop biomarkers and therapeutic tools for the diagnosis and therapy of atherosclerosis. MiRNAs represent a valuable tool for diagnosing and monitoring of cardiovascular disease.
This paper will give an overview of the current developmental progression of RNA therapeutics as a holistic approach for treating cardiovascular diseases in different animal models and clinical trials. Future interrogations are warranted for the development of miRNA-based therapeutics to overcome challenges for the treatment of the disease
 

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Publication: Mohammed Rabiul Hosen, Philip Roger Goody, Andreas Zietzer, Georg Nickenig, and Felix Jansen

MicroRNAs As Master Regulators of Atherosclerosis: From Pathogenesis to Novel Therapeutic Options; Antioxidants & Redox Signaling; 8 Jun 2020; https://doi.org/10.1089/ars.2020.8107

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Copyright 2020, Mary Ann Liebert, Inc., publishers 

Thymic stromal lymphopoietin is a key cytokine for the immunomodulation of atherogenesis with Freund's adjuvant

Adaptive immune responses regulate the development of atherosclerosis, with a detrimental effect of type 1 but a protective role of type 2 immune responses. Immunization of Apolipoprotein E-deficient (ApoE^−/−) mice with Freund's adjuvant inhibits the development of atherosclerosis. However, the underlying mechanisms are not fully understood.
Thymic stromal lymphopoietin (TSLP) is an IL7-like cytokine with essential impact on type 2 immune responses (Th2). Thymic stromal lymphopoietin is strongly expressed in epithelial cells of the skin, but also in various immune cells following appropriate stimulation.
The group of Martin Steinmetz investigated whether TSLP may be crucial for the anti-atherogenic effect of Freund's adjuvant. They found that subcutaneous injection of complete Freund's adjuvant (CFA) rapidly led to the expression of TSLP and IL1β at the site of injection. 

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Publication: Martin Steinmetz, Ludivine Laurans, Sarah Nordsiek, Lena Weiß, Bieke van der Veken, Padmapriya Ponnuswamy, Bruno Esposito, Marie Vandestienne, Andreas Giraud, Cristina Göbbel, Eva Steffen, Tobias Radecke, Stephane Potteaux, Georg Nickenig, Tienush Rassaf, Alain Tedgui, Ziad Mallat; 

Thymic stromal lymphopoietin is a key cytokine for the immunomodulation of atherogenesis with Freund's adjuvant; 

Journal of Cellular and Molecular Medicine 2020;00:1–9; DOI: 10.1111/jcmm.15235

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Location

Biomedical Center Bonn                               
Venusberg-Campus 2
53127 Bonn

(c) https://www.schloss-rheinfels.de/bildergalerie/

Join the Photoacoustic Imaging Workshop with the Vevo3000 from Fuji Visualsonic. Learn how the system works and track changes in myocardial oxygen saturation in real-time.

When? April 2, 2020 during the morning

Where? via live stream (please contac Marta Stei: marta.stei(at)ukbonn.de)

(c) https://www.visualsonics.com/product/imaging-systems/vevo-lazr-x

Aortic Valve Stenosis – From Basic Mechanisms to Novel Therapeutic Targets

Aortic valve stenosis (AVS) is the most common acquired heart valve disease in the western world. The morbidity and mortality associated with AVS is tremendous and the 2-year mortality rate is around 50%. A complex process of endothelial dysfunction, immune cell infiltration, myofibroblastic and osteoblastic differentiation and subsequently calcification leads to remodeling and thickening of the aortic valve cups. The changes results in valve obstruction. The underlying pathophysiology of calcification are still unclear and no pharmacotherapy has been established to prevent aortic valve calcification. This review summarizes the current knowledge of pathomechanisms involved in aortic valve calcification and points out novel treatment strategies.

Publication: Philip Roger Goody, Mohammed Rabiul Hosen, Dominik Christmann, Sven Thomas Niepmann, Andreas Zietzer, Matti Adam, Florian Bönner, Sebastian Zimmer, Georg Nickenig, Felix Jansen: Aortic Valve Stenosis – From Basic Mechanisms to Novel Therapeutic Targets; Arteriosclerosis, Thrombosis, and Vascular Biology 2020;40:885–900; DOI: 10.1161/ATVBAHA.119.313067

© 2020 American Heart Association, Inc.

Speaker
Prof. Bert Callewaert, University of Ghent
PD Dr. Jennifer Eßer, University of Freiburg
Prof. Stefan Offermanns, Max Planck Institute, Bad Nauheim
Prof. Hiroki Kato, University of Bonn
Dr. Christine Quast, University of Düsseldorf
PD Dr. Sebastian Zimmer, University of Bonn 
Prof. Gerhard Sengle, University of Cologne

Date and Time
March 12, 2020
12:30 - 5 pm

Location 
Lecture Hall, teaching building (no. 10) 
University Hospital Bonn
Venusberg-Campus 1

(c) Giacomo Zucca/Bundesstadt Bonn

(c) Marika Enders, Simon Görgen, Giacomo Zucca/Bundesstadt Bonn