A mechanism by which a specific protein in the body inhibits formation of new blood vessels has been identified by researchers at Uppsala University.
Inhibiting the formation of new blood vessels is said to be an important aspect of cancer treatment.
Angiogenesis, the formation of new blood vessels, is strictly regulated by a number of molecules that serve to either promote or inhibit the process. Certain diseases are characterized by excessive or insufficient angiogenesis.
The rapid growth of tumors, for example, is conditioned on the formation of new blood vessels to supply oxygen and nutrients, which explains why angiogenesis is accelerated in cancer patients.
"At present, there are five approved drugs for inhibiting formation of new blood vessels," said research fellow Anna-Karin Olsson of the Department of Medical Biochemistry and Microbiology at Uppsala University, who headed the study.
"All of these medications work in a similar way, by influencing the function of one of the agents that promotes angiogenesis. A problem with the medications is that the body develops resistance to them as treatment progresses.
"Improved knowledge about which molecules promote or inhibit the formation of blood vessels in the body, and the mechanisms by which they operate, is accordingly a research goal," Olsson added.
During the study, the research team involving scientists from Sweden, Norway, Finland and Germany investigated the function of histidine-rich glycoprotein (HRG), a plasma protein naturally present in the body.
It inhibits angiogenesis by binding to endothelial cells.
"Our findings suggest that attempting to inhibit angiogenesis is an aspect of the body's own reaction to diseases like cancer," said Anna-Karin Olsson.
"The activated platelets create a microenvironment in which the HRG fragment is able to function as an angiogenesis inhibitor," she added.
The findings revealed that "knockout" mice, which lack HRG, support this conclusion. The mice are healthy and fertile, but exhibit high levels of angiogenesis in connection with tumor growth. This finding is consistent with the hypothesis that the mice lack an angiogenesis inhibitor.
The study is published in the November issue of the journal Molecular Cancer Research.