Abstracts

We invite you to submit your abstract for poster presentation. Conference language will be English.

Abstract Submission

Abstracts can be submitted via e-mail to Henning.Morawietz@tu-dresden.de until 25 April 2018.

We are pleased to announce that the German Society for Microcirculation and Vascular Biology will support 5 Travel Awards for their members or students from laboratories of their members. The British Microcirculation Society will kindly support 2 Travel Awards. Please indicate in your application that you apply for a Travel Award.

Instructions for abstract preparation

Abstracts should be written in English.
Font: Arial 10 pt,
single-spaced.
Do not use more than one page for your abstract, please.
Title: One initial capital letter followed by lower case letters.
Use bold letters.
Author: Start new line for authors.
The presenting author should be underlined.
Address: Start new line for the address.
Structure your abstract in: Aims, Methods and results and Conclusions.

Please provide the following information:

Presenting author:
Email:

Please send your abstracts to: Henning.Morawietz@tu-dresden.de

Abstract review

The abstract selection committee will review the abstracts. 30 abstracts will be selected as poster presentations in the sessions of the meeting. Presenting authors will be notified on April 30, 2018, regarding the results of the abstract review.

Registration

The presenting author must be a registered participant. Please note that the presenting author is not automatically registered by submitting an abstract. Regular registration is obligatory and binding and implies payment of the registration fee.

An abstract example can be found here:

NADPH oxidase 4 protects against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient mice

Heike Langbein¹*, Coy Brunssen¹*, Anja Hofmann¹, Peter Cimalla², Melanie Brux¹, Stefan R. Bornstein³, Andreas Deussen⁴, Edmund Koch², Henning Morawietz¹

¹Division of Vascular Endothelium and Microcirculation, Department of Medicine III, University Hospital Carl Gustav Carus Dresden, Technische Universität Dresden, Dresden, Germany;

²Department of Anesthesiology and Intensive Care Medicine and Clinical Sensoring and Monitoring, University Hospital Carl Gustav Carus Dresden, Technische Universität Dresden, Dresden, Germany;

³Department of Medicine III, University Hospital Carl Gustav Carus Dresden, Technische Universität Dresden, Dresden, Germany;

⁴Institute of Physiology, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Germany

*Both first authors contributed equally to this study.

Aims: Endothelial dysfunction is an early step in the development of atherosclerosis. Increased formation of superoxide anions by NADPH oxidase Nox1, 2, and 5 reduces nitric oxide availability and can promote endothelial dysfunction. In contrast, recent evidence supports a vasoprotective role of H₂O₂ produced by main endothelial isoform Nox4. Therefore, we analysed the impact of genetic deletion of Nox4 on endothelial dysfunction and atherosclerosis in the low-density lipoprotein receptor (Ldlr) knockout model.

Methods and results: Ex vivo analysis of endothelial function by Mulvany myograph showed impaired endothelial function in thoracic aorta of Nox4^-/-/Ldlr^-/- mice. Further progression of endothelial dysfunction due to high-fat diet increased atherosclerotic plaque burden and galectin-3 staining in Nox4^-/-/Ldlr^-/- mice compared with Ldlr^-/- mice. Under physiological conditions, loss of Nox4 does not influence aortic vascular function. In this setting, loss of Nox4-derived H₂O₂ production could be partially compensated for by nNOS upregulation. Using an innovative optical coherence tomography approach, we were able to analyse endothelial function by flow-mediated vasodilation in the murine saphenous artery in vivo. This new approach revealed an altered flow-mediated dilation in Nox4^-/- mice, indicating a role for Nox4 under physiological conditions in peripheral arteries in vivo.

Conclusions: Nox4 plays an important role in maintaining endothelial function under physiological and pathological conditions. Loss of Nox4-derived H₂O₂ could be partially compensated for by nNOS upregulation, but severe endothelial dysfunction is not reversible. This leads to increased atherosclerosis under atherosclerotic prone conditions.