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Varicose veins, sometimes referred to as "varices" in medical jargon, are usually just a cosmetic problem if they occur as spider veins.
But in an advanced stage, they pose a real health threat. In people with a 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 properly.
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 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 creating drugs to decelerate varicose vein formation or even prevent new varicose veins from forming.
Previously no suitable experimental system existed for studying the way in which changes in the cells of the blood vessels are controlled. So Korff and his team took advantage of the fact that blood vessels in the mouse ear are clearly visible, as well as easily accessible, and began using the mouse for minor surgical procedures.
In order to artificially set off processes similar to the formation of varicose veins, they tied off a mouse ear vein with a thin thread. The elevated pressure in the vessels caused by the pooled blood led to the recognizable characteristic of varicose veins.
In addition, in the affected veins, the cells proliferated and the production of an enzyme - MMP-2 - increased. MMP-2 breaks down parts of the connective tissue of blood vessels. On the other hand, there were no signs of an inflammatory response, which is often seen in other vessel remodeling processes.
"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.
Transcription factor AP-1 regulates the activity of certain genes and is regulated by the filling pressure in the blood vessels. It in turn effectively controls the formation of varicose veins, Korff adds.
If AP-1 is inhibited, 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 another 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 cell 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, and 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.
Heidelberg University Hospital and Medical Faculty of Heidelberg University Patient Care, Research and Teaching of International Standing.Heidelberg University Hospital is among the largest and most renowned medical centers in Germany. The Medical Faculty of Heidelberg University ranges among the internationally relevant biomedical research institutes in Europe.
Original article: http://www.eurekalert.org/pub_releases/2011-11/uomm-uri110711.php