Cathy Hatcher, an assistant professor in the department of bio-medical sciences at the Philadelphia College of Osteopathic Medicine, is studying the formation of blood vessels at the embryonic stage to help understand these coronary anomalies.
Cathy Hatcher, PhD, co-directs the Cardiovascular-Renal-Pulmonary course for first year medical students at Philadelphia College of Osteopathic Medicine. Her areas of research include cardiovascular development and musculo-skeletal development. Prior to joining PCOM, Dr. Hatcher was an assistant research professor at Weill Cornell Medical College in New York. She earned a BS in Biology from the University of Georgia and a PhD in Physiology from the Medical College of Georgia, and completed her postdoctoral fellowship in Cardiac Biology at Weill Cornell. Dr. Hatcher is a member of the American Heart Association and the American Physiological Society.
The Heart’s Glue
Congenital Heart Defects and Tbx5
Congenital heart defects occur in almost 1 out of every 100 live births. About 1.8 million children and adults live with congenital heart defects in the United States and nearly 4000 die annually. Coronary vessel anomalies are one type of congenital heart defect. Although these defects are quite rare, they can have a devastating impact on individuals who may experience symptoms ranging from irregular heartbeat to reduced blood flow to the heart and even sudden cardiac death.
In an effort to determine how these congenital heart defects occur, we have studied how coronary blood vessels are initially formed during embryonic development. Our studies use genetically engineered mice to identify molecules and cell behaviors important for coronary vessel synthesis.
During coronary vessel formation, embryonic heart cells have to position themselves in the right place at the right time. This is orchestrated by master genes called transcription factors. We have studied how the Tbx5 transcription factor participates in coronary vessel formation.
It appears that Tbx5 directs certain progenitor cells to migrate toward and adhere to the primitive heart muscle in order to form the outer cell layer of the heart. This outer cell layer undergoes a transformation and begins to invade the heart muscle to form the coronary vessels.
Without Tbx5, formation of these coronary vessels is significantly impaired in our genetically engineered mice. Identification of the molecular and cellular cascade of events orchestrated during embryonic development will enable us to establish an environment conducive for coronary vessels to form.
Through these studies we hope to shed light on key developmental events that go awry and lead to the onset of congenital heart defects in order to seek therapeutic approaches for their prevention.