4 GRANTS, 1 PROFESSOR
Imagine a plant glowing to alert a passing drone that there are explosives hidden underground. This...
Read StoryWhen valves work properly in a beating heart, they open and close with ease.
But all too often those same valves thicken with calcium nodules as we age and stop working well. The usual treatment? Surgery to repair or replace a valve.
It’s not clear why nodules form, but some researchers hypothesize that remnants of cells that have undergone programmed cell death are serving as aggregation sites for calcium.
Kristen Billiar, department head and professor of biomedical engineering, will use a $154,000 grant from the American Heart Association to study that link in aortic valve disease. His two-year project will involve laboratory experiments with cells grown in flat and three-dimensional shapes.
“We don’t know why calcific nodules form, but one of the things correlated with it is programmed cell death,” says Billiar. “We can use engineering techniques in reproducible experiments and see calcium depositing in cells like it does in valves. Now we want to know, what are the mechanisms involved in that?”
Programmed cell death, also known as apoptosis, is a normal process in which a cell self-destructs and breaks apart in the body in a controlled way that avoids an immune response. Billiar, whose research has focused on the way groups of cells mechanically pull on each other in the body, will probe the process of calcification to determine whether it can be interrupted.
“If we can figure out how,” he says, “we can start thinking about treatments that could stop them from what they’re doing.”