Duke Researchers Genetically Engineer Mice To Block Heart E...( nd the neurotransmitternorepinephrin...)

nd the neurotransmitter norepinephrine regulate contraction and relaxation of arteries. When released in high doses, these hormones signal heart cells to grow by binding to receptors on the heart cell surface. Conventional methods of treating hypertension and preventing enlarged heart typically include using drugs to block these hormones such as from attaching to angiotensin II and alpha 1 adrenergic receptors on the surface of heart cells. Researchers knew that these hormones work at least in part by sending messages through their respective receptors on heart cells to the interior of the cell. There a protein called Gq acts like a relay station, receiving messages from many receptors and sending them on to the cell's nucleus, where they are translated into a message for the cell to grow larger.

Koch and his colleagues wanted to bypass the conventional method of inhibiting pressure overload enlargement by going straight to the Gq signaling protein. They studied the Gq protein and found a single segment that seemed to act like a receiver for all the various receptor messages. Koch and his research team then devised the "decoy" receiver, a small piece of a protein, also called a peptide, that mimicked the Gq receiver. Then they inserted a gene encoding the decoy into mouse embryos. The resulting transgenic mice made the decoy protein in their heart cells.

Then the researchers induced pressure overload, a mimic for high blood pressure in people, in the transgenic mice and in normal mice. The hearts of the mice with the decoy protein enlarged about 13 percent, compared to 40 percent in normal mice.

Koch and his colleagues next plan to study the effect of blocking Gq in arteries throughout the body, to see if their molecular decoy might be an effective anti-hypertension strategy, in addition to blocking enlargement of the heart.
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Contact: Karyn Hede George
Georg016@mc.duke.edu
919-684-4148
Duke University Medical Center
23-Apr-1998

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