From: Subject: Schepens scientists are first to discover angiogenesis switch inside blood vessel cells Date: Fri, 19 May 2006 13:32:10 +0200 MIME-Version: 1.0 Content-Type: multipart/related; type="text/html"; boundary="----=_NextPart_000_009D_01C67B48.A187C850" X-MimeOLE: Produced By Microsoft MimeOLE V6.00.2900.2869 This is a multi-part message in MIME format. ------=_NextPart_000_009D_01C67B48.A187C850 Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.eurekalert.org/pub_releases/2006-05/seri-ssa051806.php Schepens scientists are first to discover = angiogenesis switch inside blood vessel cells

Public = release date:=20 18-May-2006
[ | E-mail Article ]

Contact: Patti Jacobs
pjacobs12@comcast.net
617-86= 8-0077
Schepens Eye = Research=20 Institute

Schepens scientists are first to discover angiogenesis = switch=20 inside blood vessel cells

Could contribute to more targeted drugs for = diabetic=20 retinopathy, macular degeneration, cancer

Boston, MA--Scientists at = Schepens=20 Eye Research Institute, an affiliate of Harvard Medical School, are the = first to=20 discover a switch inside blood vessel cells that controls angiogenesis = (new=20 blood vessel growth). The switch, they learned, is turned on and off by = the=20 balance between two enzymes (known as PI3K and PLCg) that compete for = the use of=20 the same lipid membrane to fulfill opposite missions, growth and = regression,=20 respectively. This finding could lead to new, more targeted drugs for = diseases=20 such as cancer, diabetic retinopathy and macular degeneration. The = study, titled=20 "Regulating angiogenesis at the level of PtdIns-4,5P2," is published in = the=20 current issue of The EMBO Journal (May 17).=20

"This is a significant discovery that holds great promise for future=20 treatments," says principal investigator and senior Schepens scientist, = Dr.=20 Andrius Kazlauskas, who adds that scientists have long suspected an=20 "intracellular" switching process, but until now have known very little = about=20 it. "Current drugs focus on suppressing angiogenesis by inhibiting a = mechanism=20 outside the vessel cells, which involves the action of growth factors = such as=20 VEGF or vascular endothelial growth factor. While effective in = preventing vessel=20 growth, these drugs have little impact on existing, stable vessels," he = says.=20 "Our discovery may help design drugs that could dismantle existing = vessels by=20 targeting this switch inside the vessel cells."=20

Angiogenesis is an important natural process that can be both good = and bad=20 for the body. It restores blood flow after injury, prepares a woman's = body for=20 pregnancy and increases circulation in a damaged heart. But, it can also = nourish=20 cancer tumors and damage delicate retinal tissues when uncontrolled.=20

The angiogenic process is triggered by what the body perceives as a = need for=20 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=20 "needy area" to bind to receptors on the surface of the endothelial = cells. This=20 binding then sets off a series of signaling activities carried out by = enzymes=20 within the cells. Two of those enzymes are PI3K and PLCg, which then = search for=20 their favorite lipid to use in their respective missions. Until the = present=20 study, scientists did not know exactly what those missions were and how = they=20 were accomplished.=20

Kazlauskas and his team were determined to answer those questions. To = do so=20 they created laboratory conditions that would allow them to observe the = two=20 enzymes separately as they acted on the lipid. In a series of "in vitro" = or=20 laboratory experiments that controlled the presence of each enzyme, they = began=20 to understand the individual roles of those enzymes.=20

The research team discovered the following. When the PI3K enzyme acts = on the=20 lipid, it converts it (the lipid) into a modified form of itself, which = then=20 signals blood vessel cells to proliferate or grow. The team also found = that when=20 PLCg acts on the lipid, it cuts the lipid in two, thus preventing PI3K = from=20 using that very same lipid to promote vessel growth. Instead, they = learned, the=20 resulting two halves of the lipid trigger a series of signaling = activities that=20 caused vessels to regress and disappear.=20

The team concluded that it was the competitive relationship between = these two=20 enzymes for the lipid that was at least part of the intracellular switch = for=20 which they and other scientists have been searching. They also concluded = that=20 blood vessel growth or regression was dependent on the relative activity = of the=20 two enzymes and on the amount of the lipid within the endothelial cells. =

"Understanding this process opens a whole new avenue for treatment of = angiogenesis-related diseases," says Kazlauskas. "For instance, drugs = could be=20 designed to decrease PI3K in cancer patients or those with proliferative = diabetic retinopathy or macular degeneration, or designed to increased = it in a=20 damaged heart," he says.=20

Next steps for the research team include identifying the signaling = events by=20 which PLCg informs the vessels to undergo regression and the molecules = that=20 execute the regression command.=20

###

Schepens Eye Research Institute, an affiliate of Harvard Medical = School, is=20 the largest independent eye institute in the world.=20

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