Update

21.12.2012

Article by Suresh Babu et al. is Editors' Choice in the current issue of Science

In the current edition of Science published on 21.12.2012 the scientific journal features the article by first authors Sahana Suresh Babu and Agnieszka Wójtowicz of the group of Privatdozent Marco Cattaruzza, Division of Cardiovascular Physiology, that appeared in Science Signaling 5(254) (see below) as Editors' Choice in the field of cell biology. In this section the renowned journal presents "highlights of the recent literature".

Editors' Choice: Cell Biology - Feeling the Stretch. Science 2012;338(6114):1513

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12.12.2012

Article by Suresh Babu et al. on the cover of the online edition of Science Signaling

The December 11 online issue of “Science Signaling” features an image from an article by first authors Sahana Suresh Babu and Agnieszka Wójtowicz, former PhD students in the group of Privatdozent Marco Cattaruzza, Division of Cardiovascular Physiology, on its cover. The work, which was carried out in collaboration with researchers from the Institute of Pharmacology, Heidelberg University, and the Laboratory of Neurobiology, National Institute of Environmental Health Sciences, USA, describes the signaling pathway that activates the mechanotransducer protein zyxin in response to stretch in vascular cells.

Suresh Babu S, Wojtowicz A, Freichel M, Birnbaumer L, Hecker M, Cattaruzza M. Mechanism of stretch-induced activation of the mechanotransducer zyxin in vascular cells. Sci Signal. 2012 Dec 11;5(254):ra91 doi: 10.1126/scisignal.2003173

To directly access the article please follow the links under Publications.

12.09.2012

UCB Pharma Prize for Heidelberg physiologists

Young scientists at Heidelberg University recognised for their work on the development of varicose veins

Anja Feldner and Hannes Schroeder of the Institute of Physiology and Pathophysiology (Division of Cardiovascular Physiology), Heidelberg University, were awarded the UCB Pharma Prize at the annual meeting of the German Society of Angiology - Society for Vascular Medicine (DGA) on 12 September in Mainz. They were honored for their study on the molecular pathways involved in the development of varicose veins, which they had published as joint first authors in last year's October issue of the FASEB Journal. Their work showed that this venous disease is controlled by the transcription factor AP-1. This protein regulates the activity of genes whose products contribute to the changes in the vascular cells and the surrounding connective tissue, leading to the formation of the characteristic corkscrew veins. Using a specific animal model developed by the two biologists during their doctoral research in the laboratory of PD Dr. Thomas Korff, they could inhibit the activity of AP-1 and, as a result, the formation of varicose veins. These findings could lead to new drugs to prevent the development of varicose veins.

The UCB Pharma prize, which is worth 10 000 euros and which is awarded annually by the DGA, was shared this year. In addition to the Heidelberg winners, Dr. Nora Gatzke and Dr. Philip Hill Master of the Berlin Charité were co-recipients of the award.

The Deutsche Gesellschaft für Angiologie-Gesellchaft für Gefäßmedizin e.V. (DGA, German Society of Angiology - Society for Vascular Medicine) is a multidisciplinary medical society for the promotion of research and training in the field of vascular medicine. In collaboration with other professional societies, associations and authorities, DGA physicians aim at preventing and fighting vascular disease. The DGA informs patients and people at risk about prevention, diagnosis and treatment. With its research awards the DGA specifically promotes young scientists.

Evelyn Spalek of the team Vascular Medicine of UCB Pharma GmbH in Monheim (l.) and DGA President Prof. Ulrich Hoffmann (r.) presented the prize to Dr. Hannes Schröder and Anja Feldner.

17.10.2011

Protein causes varicose veins

Heidelberg scientists develop model for studying varicose veins/Results published in renowned journal

Varicose veins, sometimes referred to as “varices” in medical jargon, are usually just a cosmetic problem if they occur as spider veins. In their advanced stage, however, they pose a real health threat. In people with this widespread disorder, the blood is no longer transported to the heart unhindered but instead pools in the veins of the leg. This is because the vessel walls or venous valves no longer function adequately. Dr. Thomas Korff and his group at the Division of Cardiovascular Physiology (Director: Prof. Markus Hecker) of Heidelberg University’s Institute of Physiology and Pathophysiology have now shown that the pathological remodeling processes causing varicose veins are mediated by a single protein. As a response to increased stretching of the vessel wall, this protein triggers the production of several molecules promoting changes in wall architecture. The paper published in the current issue of FASEB Journal may offer a possibility for using drugs to decelerate the formation of or even prevent new varicose veins.

Previously, no suitable experimental systems existed for studying the way in which these changes in the cells of the blood vessels are controlled. For their studies, Korff and his team took advantage of the fact that blood vessels in the mouse ear are clearly visible and are also easily accessible for minor surgical procedures. In order to artificially set off processes that are similar to the formation of varicose veins, they tied off a vein with a thin thread. The elevated pressure in the vessels caused by the pooled blood led to the recognizable remodeling characteristic of varicose veins. In addition, in the affected veins, the cell proliferation rate and the production of MMP-2 increased. MMP-2 is an enzyme that breaks down the non-cellular components of the connective tissue of the blood vessels. On the other hand, there were no signs of an inflammatory response, which can be observed during other vessel remodeling processes.

Model allows agents to be tested

“Nevertheless, the cellular mechanisms that control the formation of varicose veins appear to be similar to mechanisms that orchestrate the remodeling of arteries in patients with high blood pressure,” Korff explains. The transcription factor AP-1 which regulates the activity of certain genes and thus the corresponding protein production is regulated by the filling pressure in the blood vessels and in turn controls the formation of varicose veins, Korff adds. If AP-1 is inhibited, thus prohibiting it from activating genes, the characteristic corkscrew-like varicose veins do not form and cell proliferation and the production of enzymes that break down connective tissue remain at normal levels.

In a further experiment, the group showed that the results obtained in the mouse are also valid for humans. Varicose veins that have been surgically removed from patients exhibited the same cellular and molecular changes as the varicose veins created artificially in the mouse ear. Based on these results, Korff plans more studies. “Using our model, we can now more precisely analyze the early stages of the disorder and test possible drugs for their ability to prevent varicose vein formation, which, as a result, may improve the quality of life of afflicted patients.”

According to the German Vascular League, 30 million people suffer from minor vein-related symptoms, whereby women are affected around twice as often as men.According to a health report published by the German government, 15 to 20 percent of the population has varicose veins.

Literature:

Feldner A, Otto H, Rewerk S, Hecker M, Korff T. Experimental hypertension triggers varicosis-like maladaptive venous remodeling through activator protein-1. FASEB J. 2011 Oct;25(10):3613-21. Epub 2011 Jun 17.

Contact for Journalists:

Dr. Gerd König

Universität Heidelberg

Institute of  Physiology and Pathophysiology

Division of Cardiovascular Physiology

- Coordinating Office -

Im Neuenheimer Feld 326

69120 Heidelberg

Germany

phone +49 6221 54 4067

fax     + 49 6221 54 4038

e-mail gerd.koenig@physiologie.uni-heidelberg.de

4.10.2011

Publication by the WG Korff featured on the cover of the FASEB Journal