Boston, MA--Scientists at Schepens Eye Research Institute, an affiliate of Harvard Medical School, are the first to discover a switch inside blood vessel cells that controls angiogenesis (new blood vessel growth). The switch, they learned, is turned on and off by the balance between two enzymes (known as PI3K and PLCg) that compete for the use of the same lipid membrane to fulfill opposite missions, growth and regression, respectively. This finding could lead to new, more targeted drugs for diseases such as cancer, diabetic retinopathy and macular degeneration. The study, titled "Regulating angiogenesis at the level of PtdIns-4,5P2," is published in the current issue of The EMBO Journal (May 17).
"This is a significant discovery that holds great promise for future treatments," says principal investigator and senior Schepens scientist, Dr. Andrius Kazlauskas, who adds that scientists have long suspected an "intracellular" switching process, but until now have known very little about it. "Current drugs focus on suppressing angiogenesis by inhibiting a mechanism outside the vessel cells, which involves the action of growth factors such as VEGF or vascular endothelial growth factor. While effective in preventing vessel growth, these drugs have little impact on existing, stable vessels," he says. "Our discovery may help design drugs that could dismantle existing vessels by targeting this switch inside the vessel cells."
Angiogenesis is an important natural process that can be both good and bad for the body. It restores blood flow after injury, prepares a woman's body for pregnancy and increases circulation in a damaged heart. But, it can also nourish cancer tumors and damage delicate retinal tissues when uncontrolled.
The angiogenic process is triggered by what the body perceives as a need for additional blood flow. In the case of disease, it is a mistaken need. In response, the body sends growth factors (such as VEGF) to blood vessels in the
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Contact: Patti Jacobs
pjacobs12@comcast.net
617-868-0077
Harvard Medical School
18-May-2006
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