Winston-Salem, N.C. -- Through studying pigeons with genetic heart disease, researchers at Wake Forest University School of Medicine have discovered a clue about why some patients' heart vessels are prone to close back up after angioplasty.
"We identified a regulator of genes that controls the growth of artery smooth muscle cells," said William Wagner, Ph.D., senior researcher. "Learning to modulate the uncontrolled growth of these cells could potentially solve the problem of vessels re-closing after angioplasty."
The work is reported in the August issue of Experimental and Molecular Pathology.
Angioplasty uses a balloon-like device to crush the material blocking an artery. But, within three to six months, even if a stent is placed in the artery to keep it open, the vessel becomes re-blocked in about 25 percent to 30 percent of patients. This process, known as restenosis, has been described as "over exuberant" tissue healing and involves the smooth muscle cells. It is not known why this happens in some people and not in others, but many scientists believe that genes are to blame, Wagner said.
The researchers sought to find the answer in two breeds of pigeons one that is genetically susceptible to heart attacks and heart vessel disease (white carneau) and one (show racer) that is resistant. A major difference between the two breeds is that smooth muscle cells from the heart vessels of white carneau pigeons are prone to uncontrolled growth.
"Understanding the factors that play a role in this increased cell growth may provide an opportunity to target its role in both the initial development of artery blockages and in the restenosis following angioplasty," said Wagner, a professor of pathology and fellow of the American Heart Association.
Genes "express," or produce, proteins that are used in building tissue. The process begins with "transcription," or the copying of a gene's DNA sequence.