Professor

Dr. Jennifer Sullivan

 Phone: (706) 721-9796
 Fax: (706) 721-7299
 Emailjensullivan@augusta.edu
 Office: CB-2204
 Lab: CB-2210

 

 

 

 

 

Learn more about Dr. Sullivan's Research




Education and Training

State University of New York at Geneseo, Geneseo, NY, BS in Biology, 1996

Albany Medical College, Albany, NY, MS and PhD in Cardiovascular Pharmacology, 2000

Medical College of Georgia, Augusta, GA, postdoctoral fellowship in Cardiovascular Biology and Physiology




Academic Appointments

2018-present   Professor, Department of Physiology, Augusta University

2014-2018         Associate Professor, Department of Physiology, Augusta University

2013-2014         Associate Professor, Department of Medicine, Georgia Regents University

2011-2013         Assistant Professor, Department of Medicine, Georgia Health Sciences University

2011-present    Associate member of the Department of Pharmacology and Associate member of the Vascular Biology Center

2008-2011         Assistant Professor, Vascular Biology Center, Medical College of Georgia

2006-2008         Instructor, Department of Pharmacology and Toxicology, Medical College of Georgia

2003-2006        Assistant Research Scientist, Department of Pharmacology and Toxicology, Medical College of Georgia

 



 

Research Interests

The overall goal of my laboratory is to better understand the molecular mechanisms that regulate blood pressure (BP) and renal health and function in males and females under both physiological and pathophysiological conditions. There is increasing evidence supporting a role for the immune system in contributing to the development and maintenance of hypertension. However, the majority of the studies forming the basis for our understanding of immune control of BP has been performed entirely in males.  As half of the hypertensive population is female, our lab has been actively investigating the role of immune cell activation in the control of BP in females vs. males.  Recent work has approached the question of immune regulation of BP from 2 different angles: 1) why do males have more pro-inflammatory cells and what are the implications of this and 2) why do females have more anti-inflammatory T regulatory cells (Tregs) and do greater Tregs offer protection against the development of hypertension.  Additional studies are examining sex differences in acute kidney injury using ischemia-reperfusion. Studies use a blend of whole animal approaches to measure BP, renal and vascular function with ex vivo and biochemical analyses to explore the molecule mechanisms driving sex differences in BP control and renal injury.

 



Current Projects

  1. Greater cell death in male SHR contributes to sex differences in BP: Necrosis is a pathologic form of cell death that induces an inflammatory response, and immune cell activation contributes to the development and maintenance of hypertension. Because male SHR have a higher BP and a more pro-inflammatory T cell profile than female SHR, experiments tested the hypothesis that greater necrotic cell death in male SHR exacerbates increases in BP and contributes to the pro-inflammatory T cell profile.  We found that greater necrotic cell death in male SHR exacerbates maturation-induced increases in BP with age contributing to sex differences in BP.  However, although necrosis is pro-inflammatory in both sexes, it is unlikely to explain sex differences in the renal T cell profile. Ongoing studies are further assessing the role of apoptotic cell death on BP control and the T cell profile, as well as the mechanisms driving greater necrotic cell death in males.

  2. Females have more anti-inflammatory, anti-hypertensive Tregs than males: Numerous ongoing studies are aims at better understanding both the implications for sex differences in Tregs as well as the mechanisms mediating increases in Tregs in females vs. males. Using DOCA-salt hypertensive rats we have recently shown that greater Tregs in females attenuates DOCA-salt induced increases in BP.  Depleting Tregs abolished the sex difference in BP by increasing BP only in females; depleting Tregs has no effect on BP in males.  Ongoing studies are further examining how greater Tregs lower BP in the females. We are also examining the role of nitric oxide in promoting Tregs differentiation and proliferation, as inhibition of the enzyme nitric oxide synthase prevents the ability of females to upregulate Tregs and abolishes sex differences in Tregs. Finally, we are examining sex differences in Treg recruitment. There are no sex differences in Tregs in the spleen, a lymphoid organ, and removing the spleen abolishes the sex difference in renal Tregs. Therefore understanding the mechanisms regulating immune cell recruitment could provide novel insight into how males vs. females regulate the T cell profile in key organs responsible for BP control.

  3. A chronic high-fat diet (HFD) compromises the cardiovascular protection typically observed in females:  Diets high in saturated fats are increasingly linked to the development of hypertension, yet the mechanisms by which a high saturated fat diet increases BP remain unresolved. Moreover, although young women are typically protected from hypertension relative to age-matched men, epidemiological and basic science studies suggest that this cardiovascular protection is compromised by chronic consumption of a diet high in saturated fat.   Since the adipose tissue functions as an endocrine organ that modulates immune cell recruitment/activation and BP, and T cells are central to the development and maintenance of hypertension, ongoing studies are examining the impact of a chronic HFD on BP, body fat composition, and immune cell infiltration and activation in males vs. females. Studies are using male and female Dahl salt-sensitive rats randomized to a normal-fat or high-fat diet from 5 to 15 weeks of age. To date, studies suggest that females have greater increases in BP than males, and this is associated with greater increases in percent body fat in females. These studies are ongoing.

  4. Vascular congestion is central to mediating sex differences in AKI: AKI is a major clinical problem. The prognosis of patients with AKI remains poor, and patients that recover from AKI are at increased risk for developing chronic kidney disease, cardiovascular events and all-cause mortality. Clinical and pre-clinical studies further indicate that the male gender is a risk factor for the incidence and severity of AKI. Ongoing studies are designed to better understand the mechanisms by which females are protected from renal ischemic injury. We have found that male SHR have prolonged vascular congestion in the renal medulla compared to both female SHR and normotensive male Sprague-Dawley rats. Moreover, preventing the development of vascular congestion by pre-treatment with heparin prevents the development of injury in the males. The mechanisms mediating congestion in both sexes are currently being investigated.

 




Awards and Accomplishments

2018      Mid-Career Awardee - Hypertension Council 
2017      American Journal of Hypertension's John Laragh Research Award
2017      Augusta University Faculty Senate Outstanding Faculty Award from The Graduate School
2016      Augusta University Authentic Women Leaders Pilot Pipeline Program
2016      American Journal of Physiology - Regulatory, Comparative and Integrative Physiology Star Reviewer
2015      Chair, APS Sex and Gender-Related Research Interest Group
2014      Named the 2015 APS Renal Section Young Investigator 
2013      Promoted with tenure 
2013      Selected as Associate Editor for AJP:Renal Physiology 
2013      Selected as Cardiorenal Study Section Co-Chair; American Heart Association 
2013      Named Chair of the Augusta University Women’s Health Research Interest Group in the Div. of Clinical Translational Science 
2011      Recipient of GHSU Outstanding Young Basic Science Faculty Award 
2011      Recipient of GHSU Research Institute Emerging Scientist Award 
2010      Named Fellow of the American Heart Association and the Council for High Blood Pressure Research 
2007      Recipient of Consortium for Southeastern Hypertension Control Arthur Guyton New Investigator Award 
2007      Named the APS Water and Electrolyte Homeostasis Section New Investigator 
2008      Recipient of Kidney Council New Investigator Travel Award 
2006      Recipient of Merck New Investigator Award

(Go to Pub Med)

Tipton AJ, Musall JB, Crislip GR, Sullivan JC.  Greater transforming growth factor-β in adult female SHR is dependent on blood pressure, but does not account for sex differences in renal T regulatory cells. Am J Physiol Renal Physiol, 2017, Epub ahead of print.  DOI:    10.1152/ajprenal.00175.2017

Gillis EE and Sullivan JC.  Sex Differences in Hypertension: Recent Advances. Hypertension, 68(6):1322-1327 2016.  DOI: 10.1161/HYPERTENSIONAHA.116. 06602

Taylor L and Sullivan JC.  Sex Differences in Obesity-Induced Hypertension and Vascular Dysfunction: A Protective Role for Estrogen in Adipose Tissue Inflammation?  Am J Physiol Regu, 2016, Epub ahead of print. DOI: 10.1152/ajpregu.00202.2016

Sasser JM, Brinson KN, Tipton AJ, Crislip GR and Sullivan JC.  Blood pressure, sex and female sex hormones influence renal inner medullary nitric oxide synthase activity and expression in Spontaneously Hypertensive Rats.  J Am Heart Association. 4(4); pii: e0017382015, 2015. DOI: 10.1161/JAHA.114.001738

Tipton AJ, Baban B, Sullivan JC.  Female SHR Have a Compensatory Increase in Renal Regulatory T Cells in Response to Elevations in Blood Pressure.  Hypertension, 64(3):557-64; 2014. DOI: 10.1161/HYPERTENSIONAHA.114.03512

 

Recent Lab Personnel Achievements

Karl Diaz-Sanders receives NIH-funded, highly competitive T32 training grant currently supports PhD work.
 
Riyaz Mohamed received a American Physiological Society 2021 Water & Electrolyte Homeostasis Research Recognition Award.
 
Lindsey Ramirez received a Porter Physiology Fellowship.
 
Ellen Gills was awarded a K99 from NHLBI. 
 
Lindsey Ramirez received a Martin Frank Diversity Travel Award.

Riyaz Mohamed received a research recognition award from the American Physiological Society (APS) Renal section.

Mahmoud Abdelbary and Lindsey Ramirez received 2019 Caroline tum Suden/Frances Hellebrandt Professional an Opportunity Awards.
 
 

 




Related Links

Dr. Sullivan's Faculty Profile

Link to Dr. Sullivan on PubMed

Lab Meeting Schedule

LAB PERSONNEL

Kasey Belanger
Graduate Student
Riyaz Mohamed, PhD
Assistant Research Scientist
Lindsey Ramirez
Graduate Student
 
2021 Sullivan Lab
Pictured left to right: Lindsey Ramirez, Dr. Jennifer Sullivan, Kasey Belanger, Steve Haigh, Elinor Mannon, Mahmoud Abdelbary, Dr. Paul O'Connor (2021)
 
2021 Congratulations to Dr. Mahmoud Abdelbary
Pictured left to right: Lindsey Ramirez, Sarah Ray, Dr. Jennifer Sullivan, Elinor Mannon, Kasey Belanger, Mahmoud Abdelbary, Maggie Sullivan, Dr. Ellen Gillis, Kelly Sullivan, Elizabeth Snyder, Dr. Paul O'Connor, Dr. Riyaz Mohamed (2021)
Dr. Sullivan's lab 2019Pictured left to right: Mahmoud Abdelbary, Kasey Belanger, Lindsey Ramirez, Dr. Jennifer Sullivan, Jackie Musall, Dr. Ellen Gillis, Dr. Riyaz Mohamed (2019)
 
Dr. Sullivan's lab 2016Pictured left to right: Ryan Crislip, Jackie Musall, Dr. Jennifer Sullivan, Dr. Ellen Gillis, Lia Taylor (2016)
 
Dr. Sullivan's lab Pictured left to right: Ryan Crislip, Dr. Jennifer Sullivan, A Tipton, M. Zimmerman
 
Dr. Sullivan with studentsDr. Sullivan with students