Heather Holman Honored with the NIH Ruth L. Kirschstein National Research Service Award

Heather Holman, M.D., Ph.D. candidate and graduate assistant in the Cardiovascular Lab at the Medical University of South Carolina, has been awarded the prestigious NIH Ruth L. Kirschstein National Research Service Award (NRSA). This Individual F31 Fellowship grant is designed to support promising predoctoral students with the potential to become independent, productive research scientists. The F31 fellowship aims to assist students with their dissertation research while providing valuable research training under the mentorship of a faculty advisor. This two-year award offers financial support for stipends, research-related costs, tuition, and fees.

The F31 is a mentored research training award granted to graduate students conducting research under the guidance of their mentor. Heather's primary mentor is Jeffrey Jones, Ph.D., Professor of Surgery in the MUSC Cardiovascular Lab, whose research focuses on the effects of stress-induced signaling in aortopathies. Additionally, Holman is co-mentored by vascular surgeon and Vice Chair of Research, Jean Marie Ruddy, M.D. The selection process for the F31 award evaluates the applicant, the mentors, and the scientific research, with all three factors contributing to the overall score.

Dr. Jones notes that the individual nature of this award sets it apart from other NIH-funded training grants, such as the T32, which are awarded to institutions for broader training purposes. "While both types of awards offer excellent frameworks for trainee development, the individual awards are much more prestigious," said Jones. "Heather has achieved a remarkable milestone in receiving this honor!"

About the study:

Numerous studies, among both Veterans and the general public, have shown that chronic psychological stress has been associated with poor health outcomes and increased risk of developing cardiovascular disease (CVD). Post-traumatic stress disorder (PTSD), a disorder of extreme stress, has been shown to trigger a cascade of neuronal, hormonal, and immunologic responses that can cause and exacerbate a myriad of chronic physical ailments.

Although the exact mechanism linking stress and CVD is unknown, it has been established that PTSD patients have significantly higher circulating pro-inflammatory cytokines and blood cell counts (white, red, platelets), as well as higher heart rates and blood pressures (BP) both at rest and in response to stimuli. Importantly, PTSD patients were found to have a higher prevalence of neurogenically derived resistant hypertension (17% compared to 6%).

These changes in BP, inflammatory state, and resistant hypertension are thought to be mediated, in part, by an amygdalo-hypothalamic pathway in the brain. This pathway has been shown to regulate BP and inflammation through inhibitory gamma-aminobutyric acid signaling neurons (or GABAergic circuits). In chronic stress, these circuits are attenuated leading to sympathetic overactivation.

The studies outlined in this proposal will provide evidence that stress-induced neurogenic hypertension can exacerbate pathological aortic ECM remodeling leading to the acceleration of vascular pathology and may identify a novel therapeutic to treat neurogenic hypertension. New mechanistic insights into this interconnection between the cardiovascular and nervous systems in the setting of psychological stress, and in particular PTSD, and may lead to the advancement of novel therapeutics to prevent stress associated aortopathy.