Current Trainees


Bridget Ford, PhD                (Mentors: Y Gorin and J Lechleiter)                           07/07/14 - present

Research Activities:  Overview: Dr. Ford is interested in understanding the molecular mechanisms involved in glomerular cell injury in diabetic kidney disease. In particular, her work focuses on characterizing the role of Dual oxidase 2 (Duox2), a reactive oxygen species (ROS)-producing enzyme that belong to the NADPH oxidases of the Nox/Duox family, in the pathogenesis of diabetic kidney disease. She has been able to demonstrate that ROS produced by Duox2 mediates hyperglycemia-induced glomerular cell damages.
Description of the research project: Glomerular injury is a prominent pathological feature of diabetic nephropathy (DN). In glomerular epithelial cells, also called podocytes, hyperglycemia alters slit diaphragm proteins and causes foot process effacement, apoptosis and cell detachment. Oxidative stress has emerged as an important pathogenic mechanism in the development of glomerular injury in DN. Dr. Ford has provided evidence that Duox2 is highly expressed in podocytes in vivo and in vivo and that the enzyme contributes to HG-induced ROS generation and injury in these cells. Renal Duox2 expression is markedly increased in type 1 diabetic mice and diabetic patients with DN and this is associated with enhanced oxidative stress and injury. The central hypothesis of Dr. Ford’s project is that the ROS generated by Duox2 play a pivotal role in glomerular cell, particularly podocyte, injury in the diabetic kidney. The work proposed will utilize in vitro and in vivo approaches to establish the importance of Duox2 in glomerular cell injury in the diabetic environment. We will explore the role of Duox activators (DuoxAs) in the control of Duox2 function. Genetic approaches will be used to activate or inhibit Duox2 in cultured podocytes. For the in vivo studies, we will utilize type 1 diabetic mice deficient in DuoxAs. The clinical relevance of the Duox2 and DuoxAs will be studied in kidney biopsies and urine samples from patients with DN at early or advanced stages. Characterization of Duox2 deleterious actions and identification of its upstream regulators will contribute to the design of novel therapeutic interventions and will help establish adjunct therapy to treat DN. The translational component of the proposal in diabetic patients should also help establish the value of Duox2 as a potential biological marker for DN and facilitate the design of more advanced approaches to diagnose DN.
Dr. Ford proposes to test these hypotheses by completing the following specific aims:
Aim 1. To identify specific components of the Duox2-based NADPH oxidase present in mesangial cells, investigate their regulation by HG and explore their role in mesangial cell hypertrophy and matrix production. The studies will focus on the regulation of Duox2 activity by Duox activator (DuoxA) 1 and 2.
Aim 2. To explore the role of ROS generated by Dual oxidase Duox2 in functional and structural alterations in the glomeruli of mice with type 1 diabetes. Type 1 diabetes will be induced with streptozotocin in DuoxA knockout mice that does not express functional Duox enzymes. The studies will determine if DuoxA deficiency results in amelioration of glomerular pathology associated to diabetes.
Aim 3: To determine the relevance of Duox2 as a potential therapeutic target and biological marker in kidney from patients with diabetic nephropathy. The clinical relevance of Duox2 and DuoxA will be validatedin renal tissues and urine samples from type 1 and type 2 diabetic patients at early or advanced stages of DN.

Meetings Attended/Planned:

  • September-2014 - San Antonio Postdoctoral Research Forum, UTHSCSA
  • September-2015 - 6th Annual Frontiers of Translational Science Research Day; Institute for Integration of Medicine and Science/Clinical & Translational Science Awards. UTHSCSA
  • September-2015 - San Antonio Postdoctoral Research Forum, UTHSCSA
  • September-2015 - American Society of Biochemistry and Molecular Biology Science Communication and Outreach Career Symposium, San Antonio, TX
  • May-2016 - American Society of Hypertension, Annual Scientific Meeting & Exposition, New York, NY


  • 2015 - 3rd Place Postdoctoral Research Presentation, San Antonio Postdoctoral Research Forum, UTHSCSA
  • 2016 - 1st place postdoctoral presentation, 19th Annual Medicine Research Day, UTHSCSA

Coursework/Workshops: Dr. Ford completed coursework during the Spring 2015 that included:

  • Grantsmanship and Peer Review (MEDI 6064)
  • Spotlight on Research Integrity (workshop)
  • Entering Mentoring (workshop)
  • F-Troop (workshop)
  • University Teaching Excellence Course (12 week workshop, weekly 2 hr sessions))

Professional Memberships:

  • 2014-pres - American Association for the Advancement of Science
  • 2014 – pres - National Postdoctoral Association
  • 2015 – pres - Association for Women in Science
  • 2015 – pres - American Physiological Society
  • 2015 – pres - Sigma Xi Scientific Research Society, Alamo Chapter

Tanoya Harris, PhD              (Mentors: G Aune and L McManus)                             08/22/14- present

Research Activities:  Overview:  In the United States, there are an estimated 388,500 childhood cancer survivors. They have an eight times greater risk of developing heart failure (HF) and numerous studies have documented their increased risk of cardiac death. Late cardiac complications are now a leading cause of death in survivors and attributed to prior exposure to anthracycline chemotherapies.   HF after anthracycline treatment is often clinically asymptomatic for decades after exposure. By the time ventricular dysfunction is detected it is irreversible. The necessity for a noninvasive biomarker to detect early changes induced by anthrayclines in the heart is paramount. Moreover, the molecular mechanisms that drive the progression to overt clinical disease must be identified before novel therapeutic interventions can be tested.
Many studies have indicated the central role of leptin in progression of cardiovascular disease. Leptin can attenuate cardiac contraction and induce hypertrophy in isolated cardiomyocytes. In patients with heart failure it has been demonstrated that leptin is elevated in plasma.
Our studies of early anthracycline exposure in mice using doxorubicin have characterized the impact on the cardiovascular function and lifespan. In aged mice previously treated with doxorubicin during early development, our preliminary data also shows increased circulating leptin in the serum and increased phosphorylation of STAT3 in the heart tissues of animals with HF.  These findings correlate with marked cardiac dysfunction in doxorubicin-treated animals as compared to control.   Collectively, these data are the foundation of Dr. Harris’ research proposal.
Description of the Research Project:  The overall objective of Dr. Harris’ research project is to quantify leptin levels following early treatment with doxorubicin and ascertain the downstream molecular effects in the heart tissue of mice. The overall hypothesis is that early anthracycline treatment increases circulating leptin and activates p-STAT3 in the heart, thereby modulating the progression to overt heart failure.
To test this hypothesis, Dr. Harris proposes the following aims:
Aim 1: Quantify serum leptin and myocardial p-STAT3 following acute exposure to doxorubicin in vivo.  We hypothesize that increased circulating leptin levels induce the phosphorylation of STAT3 in myocardium. Following early exposure to doxorubicin, leptin levels, STAT3, and p-STAT3 will be quantified using western blot and microscopy.
Aim 2: Identify target genes that are directly modulated by the activated p-STAT3 We hypothesize the p-STAT3 pathway is activated and contributes to HF. To test this hypothesis, we will use a candidate gene approach to measure expression of known transcriptional target genes of p-STAT3 in control versus treated mice.  Further, we will focus on gene groups with known relevance in progression to HF including hypertrophy, apoptosis, fibrosis, oxidative stress and inflammation. 
The trainee’s time is currently focused on the following activities that will facilitate the acquisition of skills and knowledge leading to successful completion of the studies proposed above:

  • Developing an independent area of laboratory research relevant to the mentor’s overall research program.  Over the course of the past year Dr. Harris has worked to develop a research plan that evaluates the mechanisms by which increased leptin levels in mice exposed to anthracyclines modulates the progression of heart failure.  She is currently preparing a fellowship grant application that will be submitted to AHA in January of 2016.
  • Dr. Harris is currently crafting a manuscript that outlines a mouse model of early anthracycline exposure.  This manuscript summarizes the key outcomes including functional changes in the heart and alterations in systemic mediators of inflammation and metabolism.
  • Perfecting the Aune laboratory expertise required to isolate cardiac myocytes from animals of all ages using Langendorff perfusion.  By closely working with lab personnel, Dr. Harris has played a central role in constructing the equipment and troubleshooting the perfusion and myocyte isolation protocol.  In collaboration with the laboratory of Dr. Rong Li, the trainee has isolated pure myoctyes that have been utilized for pilot studies measuring changes in gene expression in mice treated with anthracyclines.
  • Dr. Harris participates in weekly lab meetings and presents an update on her lab experiments and future plans.  She further attends quarterly lab ethics discussions and quarterly lab journal clubs.  All trainees in the Aune lab are expected to present once each at ethics discussion and journal club.

Meetings Attended/Planned:

  • September-2014 - San Antonio Postdoctoral Research Forum, UTHSCSA
  • November-2014 - American Heart Association, Chicago, IL
  • April-2015 - 6th Annual Frontiers of Translational Science Research Day, UTHSCSA
  • June-2015 - International Conference on Long Term Complication of Treatment of Children and Adolescents for Cancer, Arlington, VA
  • September-2015 - San Antonio Postdoctoral Research Forum, UTHSCSA, San Antonio TX
  • April-2016 - Experimental Biology, San Diego, CA
  • September-2016 - San Antonio Postdoctoral Research Forum, UTHSCSA, San Antonio, TX
  • November-2016 - American Heart Association


  • 2016 - Travel award; FASEB/MARC, to attend Experimental Biology meeting in San Diego
  • 2016 - Travel Award; American Heart Association Cardiovascular Outreach Award, to attend the AHA annual meeting in Phoenix, AZ

Professional Memberships:

  • 2014-pres - American Physiological Society (2014)
  • 2014–pres - America Heart Association (2014)
  • 2015-pres - Sigma XI (2015)
  • 2015-pres - American Association for Cancer Research (2015)

Coursework/Workshops: Dr. Harris completed coursework during the Spring 2015 that included

  • Grantsmanship and Peer Review (MEDI 6064)
  • Spotlight on Research Integrity (workshop)
  • F-Troop (workshop)

Grant applications written/submitted. Dr. Harris submitted an application for an individual postdoctoral fellowship to the AHA in January 2016; this application was not funded.

Chase Carver, PhD              (Mentors: M Shapiro and B Clark)                              09/01/15 - present

Research Activities: Dr. Carver joined the Department of Physiology at the UTHSCSA as a postdoctoral researcher under the supervision of Dr. Mark S. Shapiro in Fall 2015. His focus has been to study voltage-gated ion channel physiology and correlated neurological dysfunction in determining heretofore unknown mechanisms of epileptogenesis in the hippocampus. The aim of his current research is to investigate “M-type” (KCNQ) K+ channels in hyperexcitability, since KCNQ2/3 channels are responsible for M-current to maintain homeostatic control over the neuronal resting membrane potential and firing frequency. Dr. Carver is currently investigating the interaction of muscarinic acetylcholilne receptors and M-channels in the dentate gyrus using electrophysiology and super resolution microscopy. He formed a hypothesis that in dentate gyrus granule cells, increased muscarinic actylcholine receptor activity at the axon initial segment results in greater seizure susceptibility via depression of M-current. This study will be tested by molecular expression, neuronal imaging, electrophysiology, and behavioral studies in mice. He is using novel transgenic tools in order to investigate mechanistic modulation of activities that originate in the dentate gyrus.

In the above studies, Dr. Carver is receiving training in new technical expertise as follows:

  • Total Internal Reflective Fluorescence Microscopy and Imaging
  • Super Resolution STORM Imaging
  • Immunocytochemistry and Immunohistochemistry using heterologous expression systems
  • DREADD (Drug Receptor Exclusively Activated by Designer Drug) delivery in vivo for molecular expression and pharmacological assays

Meetings Attended/Planned:

  • 2015 - San Antonio Postdoctoral Research Forum, UTHSCSA, San Antonio, TX
  • 2015 - American Epilepsy Society, Annual Meeting, Philadelphia, PA
  • 2016 - San Antonio Postdoctoral Research Forum, UTHSCSA, San Antonio, TX


Research Presentations:

  • September-2015 - Perimenstrual Upregulation of δ-subunit GABAA Receptors Mediating Tonic Inhibition and Neurosteroid Sensitivity. San Antonio Postdoctoral Research Forum. UTHSCSA
  • December-2015 - Role of Tonic and M Currents in the Hippocampal Dentate Gyrus in Controlling Neuronal Excitability and Seizure Susceptibility. American Epilepsy Society, Annual Meeting, Philadelphia, PA (platform presentation)


  • 2015 - American Epilepsy Society Postdoctoral Fellow, American Epilepsy Society

Professional Organizations

  • 2012-pres - Society for Neuroscience
  • 2014-pres - American Epilepsy Society

Coursework/Workshops:  Dr. Carver actively participated in workshops during the Fall 2015 / Spring 2016 that included:

  • Spotlight on Research Integrity (workshop)
  • F-Troop (workshop)

Grant applications planned: Dr. Carter submitted an F32 grant application for the April 2016 NIH deadline. This application was not funded and a resubmission is in development. 

Stacey N. Lee, PhD              (Mentors: J Lechleiter and Mark Shapiro)                            05/01/16 – present
Stacey LeeResearch Activities: Dr. Lee’s primary research project will be to define and develop the neuroprotective efficacy of thyroid hormone – like (THL) compounds in vitro and in whole animals after cerebral ischemic stroke. These studies are based on the fact that tissue plasminogen activator (tPA) is the only FDA-approved drug for dissolving blood clots leading to stroke; however, it has to be administered within 4 hours of stroke. Hence, novel therapeutic strategies are urgently required. Dr. Lechleiter’s lab has found that mice treated with active thyroid hormones, triiodothyronine (T3) or diiodthyronine (T2), manifest significantly reduced cerebral infarcts after stroke. Interestingly, T3-mediated protection after stroke appears dependent on the mitochondrial trifunctional protein (MTP), an octomeric enzyme complex that facilitates fatty acid oxidation (FAO). In addition, lesion size is significantly increased by pharmacological and genetic approaches that inhibit FAO and/or deplete MTP expression. Immunohistochemistry shows that MTP is expressed almost exclusively in astrocyte mitochondria in the mouse brain. In vitro, T3-mediated increases in cell viability and ATP production are also dependent on the stimulation of FAO and the presence of MTP. Importantly, T3-mediated induction of neuroprotective pathways is conserved in ex vivo human brain tissue. Taken together, Dr. Lechleiter has formulated a central hypothesis:T3 protects the brain after stroke by promoting FAO in astrocytes and thereby enhancing their energy dependent neuroprotective functions”. In accordance with this hypothesis, he has already screened a library of 500 pyrazole-based compounds for their ability to rapidly (within 15 minutes) stimulate ATP production in cultured human astrocytes. Of over 25 novel small molecules identified, ~12 compounds exhibited an EC50 greater than or equivalent to T3. Dr. Lee’s research project will be centered on these 12 compounds and the following two Specific Aims:
1) Define the protective efficacy of thyroid-hormone like (THL) compounds in vitro and in vivo.
2) Determine the dependence of each THL compound on FAO for their neuroprotective efficacy.

Dr. Lee is receiving significant new technical training in addition to standard cellular and molecular techniques (e.g., immunocytochemistry, western blotting, cell extraction and culturing). She is learning to use high throughput cell screening in our Center for Innovative Drug Design (CIDD) core using the Perkin Elmer Operetta imaging system ( She is also an important, hands-on participant in the structure-activity analysis of positive-hit compounds that exhibit neuroprotection. Optimization of lead compounds is a critical part of pharmaceutical drug development, and is a component of the CIDD core facility that is directed on the UTSA campus by Dr. Stan McCarty, a medicinal chemist ( Another new training component that Dr. Lee will receive is in vivo optical imaging of the live mouse brain. She will use this technique to test the efficacy of selected THL compounds to treat photothrombosis-induced stroke at different timepoints.

Meetings Attended/Planned:

  • 2016 - San Antonio Postdoctoral Research Forum, UTHSCSA, San Antonio, TX

Coursework/Workshops: Dr. Lee is presently attending workshops that include:


  • Spotlight on Research Integrity (workshop)
  • F-Troop (workshop)

Nathan Mitchell, PhD                 (Mentors: G Toney and J Stockand)                           07/15/16 - present
Nathan MitchellResearch Activities: Innovative research efforts will combine Dr. Mitchell’s prior investigations in the development of novel anti-depressant drug efficacy via the function and ontogeny of organic cation transporters to examine the poorly understood comorbidity between cardiovascular diseases such as arterial hypertension and mood disorders such as depression.  In Dr. Toney’s laboratory, he will explore the neurobiological underpinnings of this comorbidity using new skills that include in vivo single neuron recording and patch clamp electrophysiology in brain slices. These research efforts will address the hypothesis that high salt intake is a critical link between depression and salt-sensitive hypertension; according to this hypothesis, hyperexcitability and hyperactivity of sympathetic and mood controlling neurons will have common molecular triggers, including IL-17a which is a potent inducer of microglial activation. It is anticipated that as microglia become activated, foci of neuroinflammation gradually spread and disrupt mechanisms that maintain synaptic homeostasis.  Because synaptic mechanisms that control sympathetic activity and those that control mood are different, the hypothesis is that common components within the proinflammatory milieu of sympathetic and mood controlling brain regions will nevertheless induce distinct cellular responses such that synaptic adaptations among pro-hypertensive neurons will be largely distinct from those that lead to depression. These studies will employ a well-established animal model of salt-sensitive hypertension.