The study, reported in the Nov. 21 issue of Science, sheds light on the role of T-type calcium channels in coronary artery relaxation and may provide insight into causes of some types of coronary artery disease.
Calcium channels are proteins that allow calcium ions to flow into cells. This influx of calcium plays a role in many important cell functions including muscle contraction.
Previous research suggesting that T-type calcium channels may be involved in cellular events critical for muscle regeneration made this protein an interesting target for the UI team led by Kevin Campbell, Ph.D., professor and interim head of physiology and biophysics, professor of neurology in the UI Roy J. and Lucille A. Carver College of Medicine, and a Howard Hughes Medical Institute (HHMI) investigator.
However, when the researchers genetically engineered mice to lack the T-type calcium channel, the mice did not have skeletal muscle defects. Instead, the mice developed cardiomyopathy, or damaged heart muscle.
"Loss of the protein caused heart disease in the mice," Campbell said. "But T-type calcium channels are not expressed in normal adult heart muscle cells, they are expressed in the smooth muscle that surrounds the heart's blood vessels. This suggested that the problem might lie in the smooth muscle tissue."
Chien-Chang Chen, Ph.D., UI postdoctoral fellow in Campbell's lab and first author of the study, took a closer look at the coronary arteries in mice without the calcium channel. He and his colleagues found that the coronary arteries were abnormally constricted and misshapen.
Chen and Kathryn Lamping, Ph.D., UI associate professor of internal medicine and pharmacology and a member of the Iowa Cardiovascular Cente
Contact: Jennifer Brown
University of Iowa