New mechanism that regulates formation of blood vessels found

November 18th, 2008 - 5:15 pm ICT by ANI  

Washington, Nov 18 (ANI): Portuguese scientists have found a novel mechanism which regulates the process whereby new blood vessels are formed and wounds heal, including chronic wounds, such as those found in diabetic patients and those suffering from morbid obesity.

The findings by researchers in one of the external groups of the Instituto Gulbenkian de Ciencia (IGC), in Portugal, have implications for the development of new therapies to healing damaged blood vessels and building new ones.

Led by Sergio Dias, the team was working at the Centro de Investigacao e Patobiologia Molecular of the Portuguese Institute of Oncology Francisco Gentil, in Lisbon.

It was found that an intracellular signalling pathway, mediated by the protein Notch stimulate the cells that make new blood vessels (called endothelial cells).

The formation of new blood vessels is a crucial step in wound healing: the newly-formed vessels allow anti-inflammatory proteins to reach the wound site, improve oxygenation of the damaged tissue and carry essential nutrients for the re-structuring of the tissue, that is, the skin.

“We knew that the endothelial cells are stimulated by cells originating in the bone-marrow, the so-called bone-marrow derived precursor cells. We have now shown that the actual stimulus happens through the Notch protein, found on the bone-marrow derived cells. Upon activation, Notch promotes the adhesion of the precursor cells to the site of the lesion, where they stimulate the endothelial cells to make new blood vessels, said Francisco Caiado, a PhD student at the IGC, and first author of this study.

Chronic skin wounds are an increasing medical problem, since they are commonly found in diabetic patients and in those suffering from morbid obesity.

Diabetic patients may develop “diabetic foot”, a condition whereby wounds do not heal leading, in the most severe cases, to amputation.

The study is set to appear in the new issue of the journal PLoS ONE. (ANI)

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