In what is believed to be the largest review of the human genetic code to determine why some people's blood platelets are more likely to clump faster than others, scientists at Johns Hopkins and in Boston have found a septet of overactive genes, which they say likely control that bodily function.
"Our results give us a clear set of new molecular targets, the proteins produced from these genes, to develop tests that could help us identify people more at risk for blood clots and for whom certain blood-thinning drugs may work best or not," says co-senior study investigator and cardiologist Lewis Becker, M.D.
"We can even look toward testing new treatments that may speed up how the body fights infection or recovers from wounds," says Becker, a professor at the Johns Hopkins University School of Medicine.
Platelets are key to fighting infection and sealing wounds and, adversely, can speed up cardiovascular diseases that can lead to potentially fatal heart attacks or strokes.
Reporting in the issue of Nature Genetics online June 7, researchers tested the platelet "stickiness" in blood samples from some 5,000 American men and women and compared the results to some 2.5 million single possible changes in the human genetic code to see which genes stood out across the entire group as speeding up or slowing down platelet clumping. Study participants included both whites and blacks with no previously known chronic health problems, representing what researchers say is "a solid cross-section of American society."
Seven genes were found on their own to be hugely significant in affecting how fast or how long it took for platelets to stick together or how many platelets would clump. (The seven were more than 500 million times more likely than other genes to impact clumping, whereas the next most influential genes, a set of 15, were found to be 10,000 times more likely to affect clumping function.)
According to Becker,
|Contact: David March|
Johns Hopkins Medical Institutions