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Cardiovascular Research Lab
The Cardiovascular Research Lab is
located on the second
floor in the R&E Building. Dr. Guy Reed and his colleagues, Dr. Inna Gladysheva and Dr.
Irina Sazonova, are looking at the body’s natural mechanism for making
and destroying clots to find more potent and safe ways to reduce
mortality rates.
The search has yielded design of monoclonal antibodies
that inactivate a natural inhibitor of the clot-dissolving enzyme plasmin. Plasmin is the enzyme that cuts up clots and inactivating its
inhibitor makes it last longer. “This is a way of tweaking the body’s
control system so the enzyme can be more active,” Dr. Reed explains.
A company in Boston is helping slightly modify the
mouse monoclonal antibodies that “work like a charm and are
extraordinarily specific” into human versions that can be pioneered into
clinical use at MCG.
Another critical part of the clotting process is sticky
proteins secreted by platelets. The researchers are studying genetically
modified mice unable to secrete these proteins; the mice simply don’t
make clots. Identifying the genes that regulate the secretion process
enables Dr. Reed and his colleagues to screen for compounds that
interfere with secretion of the sticky stuff as well as better
understand how platelets stick together.
The goal is balance and finding better tools to safely
manage a potentially deadly clot without risky consequences such as
bleeding that can occur with current treatment. “You want a clot to
patch the wall, but you don’t want it to get so big it occludes the
artery. What keeps it from getting so huge is this process of clot
dissolution called fibrinolysis,” he says of the body’s natural
mechanism for dissolving clots. “If you can turn on that enzyme or keep
it from being inhibited, you can cause the body itself to degrade the
clot. If you can both facilitate the process of dissolution as well as
one that inhibits clot formation, you solve the problem.”
He also is tackling the increasingly common result of
surviving a heart attack: heart failure. “Heart failure is the most
rapidly increasing discharge diagnosis in the country,” says Dr. Reed.
A heart in failure is an oversized, boggy muscle
that no longer beats adequately. “It leads to sodium and water
retention, to fluid in the lungs, to not being able to breathe. That is
the scary part,” says Dr. Reed.
Studies with his Harvard colleagues of congenital heart
defects resulted in a transgenic mouse that is enabling his heart
failure studies. Different strains of mice are like different races of
humans, and the researchers have found that some strains have delayed
onset of heart failure. He hopes this finding will shed light on how and
why the heart takes the steps from damage to failure.
Our Cardiovascular Research Lab currently has two NIH
Program Project grants, one dissecting the relationship between
hypertension and inflammation and the other putting together key
contributors to hypertension, including stress, genetics, sodium
retention and fitness in order to better define the role of each. These
collaborative initiatives complement numerous others in everything from
sickle cell disease to angiogenesis in places such as the Vascular
Biology Center, the Georgia Prevention Institute, the Departments of
Physiology and Biochemistry and Molecular Biology and the Institute of
Molecular Medicine and Genetics.
