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5 December 2013 11:26 am ,
Vol. 342 ,
Researchers have been hot on the trail of the elusive Denisovans, a type of ancient human known only by their DNA and...
Thousands of scientists in the Russian Academy of Sciences (RAS) are about to lose their jobs as a result of the...
Dyslexia, a learning disability that hinders reading, hasn't been associated with deficits in vision, hearing, or...
Exotic, elusive, and dangerous, snakes have fascinated humankind for millennia. They can be hard to find, yet their...
Researchers have sequenced and analyzed the first two snake genomes, which represent two evolutionary extremes. The...
Snake venoms are remarkably complex mixtures that can stun or kill prey within minutes. But more and more researchers...
At age 30, Dutch biologist Freek Vonk has built up a respectable career as a snake scientist. But in his home country,...
Since arriving on the island of Guam in the 1940s, the brown tree snake ( Boiga irregularis ) has extirpated native...
- 5 December 2013 11:26 am , Vol. 342 , #6163
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Longer Life for Bypass Grafts?
24 January 2000 7:00 pm
A two-fisted protein slows the clogging of veins grafted into pig arteries. The finding, reported in tomorrow's Circulation, raises the prospect of gene therapy that could help people who've had coronary bypass surgery avoid a second operation.
In as few as 10 years, veins grafted into the heart often clog as badly as the diseased arteries they're meant to replace. Trouble starts when enzymes called matrix metalloproteinases (MMPs) eat away the scaffolding that attaches muscle cells to the vein walls. Freed to spread and multiply, the muscle cells build up and narrow the graft. The constriction traps fatty deposits, eventually narrowing enough to bring on a heart attack. Researchers led by Sarah George, a biologist at the University of Bristol, United Kingdom, knew that a protein called TIMP-3 can slow the migration of muscle cells by taking MMPs out of action, and instructing those cells that do break free to self-destruct.
George and her colleagues used a virus to insert the gene for TIMP-3 into cells of a portion of human vein kept in tissue culture. After 14 days, the protein had bound itself to the matrix surrounding the cells in the vein walls and had put the kibosh on MMP activity. The result: 84% less narrowing than in control veins. And as they had expected, the itinerant muscle cells committed suicide before getting the chance to create obstructions. The researchers next put veins from a dozen pigs through the TIMP-3 treatment, then grafted them into the animals' carotid arteries. After 28 days, the treated grafts showed 58% less narrowing than controls. Again, the researchers found plenty of TIMP-3 in the vein walls, little MMP activity, and evidence of muscle cell suicide.
While the results are promising, George warns that a gene therapy for people is not a sure thing. "We need to do longer term studies before we can think of moving to clinical trials," she says. Joseph Loscalzo of Boston University agrees. In an editorial also appearing in Circulation, Loscalzo writes, "[the findings] represent a proof of principle for vascular gene therapy." But he warns that it is too early to say whether TIMP-3 prevents graft clogging or merely delays it.