ISB Researchers Find Molecular Link Between Simulated Post-traumatic Stress Disorder and Physical Heart Damage
In a study published online on Feb. 10 in the Proceedings of the National Academies of Science (PNAS), researchers at the Institute for Systems Biology and the U.S. Army Center for Environmental Health Research present molecular evidence that exposure condition similar to that experienced in posttraumatic stress disorder (PTSD) can cause heart tissue damage in mice.
PTSD can develop as a result of experiencing one or more traumatic events, such as natural disasters, physical assault and military combat environment. Affecting about 7 percent of the population in the United States, PTSD is one of the most common psychological conditions. Patients with PTSD have a higher risk of cardiovascular conditions, including high blood pressure, elevated cholesterol levels and stroke.
Previously, heart disorders related to PTSD were mostly thought to be anxiety-induced. Similarly, in the condition known as Da Costa syndrome (or “soldier’s heart” reported during the American Civil War), patients display symptoms of heart disorders such as palpitations and chest pain but show no apparent physical abnormalities upon examination.
ISB researchers used a systems approach to study how stress affects organs such as the heart in a PTSD mouse model. After the researchers paired subservient mice with aggressive mice, the socially-stressed mice displayed symptoms similar to PTSD patients, including avoidance behavior, weight gain and decreased memory. Further examinations of gene expression from heart tissues in the social defeated mice revealed increased cellular processes related to immune responses and active tissue repair.
Future research interests include investigating the long-term effects of stress and genetic factors involved in stress-associated heart injury. Using this PTSD mouse model may also lead to developing methods for early diagnosis and insights on therapeutic approaches for treatment.
This article was originally published in Molecular Me, the news blog for the Institute of Systems Biology on 19 February 2014.