小蝌蚪APP

Troy Stevens, Ph.D.

Lenoir Louise Locke Chair of Physiology and Cell Biology
Professor

Ph.D.: Colorado State University
Post-doctoral: University of Colorado

Phone: (251) 460-6056
tstevens@southalabama.edu 

Biographical Sketch [PDF]

 

Lab Focus

The Stevens lab has had a long-standing interest in mechanisms pertaining to endothelial cell heterogeneity, particularly in the lung.  Our work focuses on molecular mechanisms that account for unique endothelial cell behaviors in pulmonary artery, capillary and vein endothelium.  Chief among these interests is a systematic study of:  barrier function, neo-angiogenesis, vasoreactivity, and site-specific host-pathogen interactions, not only pertaining to how microorganisms interact with endothelium along the vascular axis, but how toxins access intracellular compartments and uniquely modify the behavior of pulmonary artery, capillary and vein endothelium. A principal goal of these studies is to understand how vascular disease manifests in discrete vascular locations and resolve novel molecular signatures that can be exploited to target therapy to the appropriate vascular site.

 

Lab Team

Mikhail Alexeyev, Ph.D. 

Associate Professor

Postdoctoral Studies: Texas Heart Institute
Ph.D.: National Academy of Sciences of Ukraine, Kiev

 

Lab Focus

As the principal sites of cellular energy generation, mitochondria are intricately involved in all cellular processes in both health and disease. Virtually all diseases are accompanied by mitochondrial dysfunction, but mitochondrial dysfunction features most prominently in a group of so-called mitochondrial disorders. These disorders have been recognized for less than for decades, and thus far, no cure or effective treatment is available. A significant fraction of these disorders are caused by mutations in mitochondrial DNA (mtDNA), the only DNA found in human cells outside of the nucleus.

Animal models are instrumental for understanding disease mechanisms and developing new therapeutic modalities. The current lack of effective treatments for mitochondrial disease is directly attributable to the unavailability of faithful mouse models of mitochondrial disease caused by mutations in mtDNA.

Therefore, my lab鈥檚 focus is on improving our understanding of mtDNA maintenance, replication and mutagenesis, and using this newly acquired understanding towards generating mouse models of mitochondrial disease. We seek to uncover the genetic determinants of the Interspecies Barrier for mtDNA Replication (IBMDR), which will allow us to reconstitute a human electron transport chain in mice. The resulting 鈥渉umanized鈥� mice could be used as a novel, faithful platform for modeling human mitochondrial diseases using patients鈥� blood as a source of mutant mtDNA.

 

Lab Team

Stephen T. Ballard Ph.D. 

Professor Emeritus

B.S.: North Carolina State University
M.S.: University of Kentucky
Ph.D.: University of North Carolina

sballard@southalabama.edu

 

Thiago Bruder, Ph.D.

Assistant Professor

Ph.D.:  Medical School of Ribeirao Preto 鈥� University of S茫o Paulo, Brazil

Postdoctoral: Augusta University

tbruder@southalabma.edu  

Biographical sketch [PDF]

Lab Focus

Cardiovascular disease (CVD) is the leading cause of death globally. It includes a range of conditions affecting the heart and blood vessels, such as coronary artery disease, heart attacks, and stroke. Various factors, including lifestyle choices, genetics, and other health conditions, contribute to its prevalence, highlighting the importance of awareness and prevention.

The Bruder lab is committed to investigating the molecular and cellular mechanisms involved in the development and progression of CVD, as well as discovering both therapeutic and non-therapeutic approaches to mitigate its effects. Our research primarily focuses on the endothelium and its derived factors in regulating vascular tone, inflammation, remodeling, and end-organ damage. We also examine the interactions between vascular cells and the immune system to identify key molecules involved in this communication and the onset of CVD.

To accomplish our goals, we employ advanced techniques to evaluate vascular function, structure, and blood pressure, alongside various molecular methods for manipulating gene expression and conducting omics analyses. Additionally, we utilize genetically engineered mouse models to gain deeper insights into these cellular and molecular processes.

Our research is organized into two main areas: arterial hypertension and Kawasaki disease. Below, you will find detailed information on each of these projects, along with related publications.

Arterial Hypertension

Arterial hypertension, commonly known as high blood pressure, is a condition where the force of blood against the walls of the arteries is consistently too high. This can occur when the heart pumps more blood than usual or when the arteries narrow and resist blood flow. Persistent hypertension can lead to serious health issues, including heart disease, stroke, kidney damage, and other complications. It is typically diagnosed through blood pressure readings, and management often includes lifestyle changes and, in some cases, medication to help lower blood pressure and reduce the risk of associated health problems.

Our lab is dedicated to understanding the autocrine endothelial mechanisms that regulate blood pressure. In a recent study published in the Journal of the American Heart Association (JAHA) in 2023, we showed that progranulin, a key molecule involved in neuroplasticity, plays a crucial role in controlling vascular function and blood pressure by directly influencing endothelial nitric oxide synthase activity. Additionally, we found that CCL5 and its receptor CCR5 are significant contributors to aldosterone-induced hypertension, vascular injury, and renal damage, with our findings featured on the cover of Hypertension in April 2024. Currently, we aim to identify the molecular factors produced during arterial hypertension that may have harmful or protective effects on cardiovascular health.

Kawasaki disease 

Kawasaki disease is a rare but serious inflammatory condition that predominantly affects children. It leads to inflammation in the walls of blood vessels throughout the body, including the coronary arteries, which supply blood to the heart.

Using a mouse model of Kawasaki disease that closely mimics human vasculitis, we aim to clarify the molecular and cellular mechanisms involved in the progression of this condition. Recently, we made a significant observation that endothelial dysfunction occurs before the onset of severe vasculitis, suggesting that endothelial cells may be the primary targets of the disease. For more information, please refer to our manuscript published in Shock in 2023. Our lab is now concentrating on understanding how endothelial cells detect and contribute to the development of vasculitis.

If you would like to learn more about our research or are interested in trainee opportunities in our lab, please contact Dr. Bruder at tbruder@southalabama.edu.

Lab Team

Ariane Bruder, Research Associate II

Rafael M. Costa, Postdoctoral Fellow

Renata Azevedo M. Luvizotto Nascimento, Visiting Scholar

Andre F. Nascimento, Visiting Scholar

Michael V. Cohen, M.D. 

Professor

M.D.: Harvard Medical School
Cardiology Fellowship: Peter Bent Brigham Hospital, Boston, MA

Phone: 251-460-6812
Fax: 251-460-6464
mcohen@southalabama.edu

 

James M. Downey Ph.D. 

Professor Emeritus

Ph.D.: University of Illinois
Postdoctoral Studies: Harvard Medical School

Phone: 251-460-6818
Fax: 251-460-6386
jdowney@southalabama.edu

 | Full CV [PDF]

 

Christopher M. Francis, Ph.D.

Assistant Professor

B.S.: Physics, Auburn University
Ph.D.: Physiology, 小蝌蚪APP
Postdoc: Physiology and Cell Biology, 小蝌蚪APP

Phone: (251) 460-7004 
michaelfrancis@southalabama.edu

Biographical Sketch [PDF]

 

Lab Team

Ji Young Lee, M.D., Ph.D.

Associate Professor

Medical Degree: Pusan National University, Pusan, South Korea
Residency: Lincoln Medical and Mental Health Center, Bronx, NY
Fellowship: 小蝌蚪APP College of Medicine
Postdoctoral Studies: 小蝌蚪APP College of Medicine

jlee@health.southalabama.edu

Biographical Sketch [PDF]

 

Lab Focus

pH homeostasis is critical to normal cell function. My laboratory studies fundamental mechanisms of pH regulation in pulmonary endothelial cells, with a broad aim to develop novel diagnostic and therapeutic strategies to treat pulmonary vascular diseases.

 

Lab Team

Mike T. Lin, Ph.D.

Professor

B.S.: Biochemistry, University of British Columbia
Ph.D.: Physiology, Loma Linda University
Postdoc: Oregon Health and Science University

mlin@southalabama.edu

Biographical Sketch [PDF]

 

Lab Focus

The Lin laboratory currently studies the lung-brain axis.  We focus on the mechanism and disease progression that initiate in the lung and result in neurological deficits.  Our work highlights the significant number of patients who suffer from neurocognitive problems in the aftermath of their recovery from a primary lung infection.  

 

Lab Team

Chung-sik Choi
Research Associate II

Thomas M. Lincoln, Ph.D. 

Professor Emeritus

Ph.D.: University of Tennessee, Knoxville
Postdoctoral Studies: Vanderbilt University

Phone: 251-460-6428
Fax: 251-460-6967
tlincoln@southalabama.edu

 

Jamie Meegan, Ph.D. 

Assistant Professor

Ph.D: University of South Florida

Postdoctoral: Vanderbilt University Medical Center

jmeegan@southalabama.edu  

Biographical sketch [PDF]

Lab Focus

Our lab aims to identify novel signaling mechanisms regulating microvascular endothelial hyperpermeability during sepsis that have potential to be targeted therapeutically for the prevention or treatment of sepsis-induced organ dysfunction.

Lab Team

Vivian Eberly, Research Technologist I

Amy R. Nelson, Ph.D.

Associate Professor

Ph.D.: University of Alabama at Birmingham
Postdoctoral Studies: University of Southern California

arnelson@southalabama.edu

Biographical Sketch [PDF]

 

Lab Focus

The Nelson lab is currently investigating whether Alzheimer's disease related amyloid-beta causes brain pericytes to contract, reducing cerebral blood flow and compromising blood-brain barrier integrity. Also, we are investigating pathways of pericyte degeneration and blood-brain barrier dysfunction in Alzheimer鈥檚 disease and are particularly interested in post-translational modifications and expression level changes of key receptors at the blood-brain barrier. Additionally, we recently started new studies examining if infections play a role in Alzheimer鈥檚 disease.

 

Lab Team

James C. Parker, Ph.D. 

Professor Emeritus

Ph.D.: University of Mississippi Medical Center
Postdoctoral Studies: University of Mississippi

Phone: 251-460-6826
Fax: 251-460-6464
jparker@southalabama.edu 

 | Full CV [PDF]

 

Kayla V. Pavlick, Ph.D. 

Assistant Professor

kvpavlick@southalabama.edu 

Ph.D.: University of Mississippi Medical Center

Full CV [PDF]

Dr. Pavlick is also an assistant professor in the Division of Medical Education. Her duties include the design and delivery of the pre-clerkship phase curriculum linked to the anatomical sciences with a focus on neuroscience. In addition, she focuses on ways to improve medical education for both students and faculty through the implementation of modern pedagogical practices and learning theory. 

Sarah Sayner, Ph.D. 

Professor

Ph.D.: 小蝌蚪APP
Postdoctoral Studies: University of Cambridge England and 小蝌蚪APP

 

Research Summary

The pulmonary endothelial barrier is critical to efficient gas exchange to supply the body with oxygen.  This single cells layer acts as a barrier restricting the flux of blood components from the vascular space into the underlying tissue.  Damage to the endothelial barrier is a characteristic feature of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

One of our areas of interest is compartmentalized cAMP signals in regulation of this pulmonary endothelial barrier.  While cAMP signals generated at the plasma membrane are barrier protective, cAMP signals generated in the cytosolic compartment by bacterial toxins are barrier disruptive.  We are further exploring compartmentalized cAMP signals by investigating the role of the recently identified mammalian soluble adenylyl cyclase (AC10 or sAC) in regulation of the endothelial barrier.  This enzyme is stimulated by bicarbonate to generate cytosolic cAMP, yet its role in the physiology of the endothelium is unknown.  Further, we are investigating how extracellular bicarbonate transits the plasma membrane to stimulate AC10.  Thus, our second area of interest is in bicarbonate transporters in the pulmonary endothelium.  We are interested in these transporters not only for the regulation of AC10, but we are also investigating how bicarbonate influx through these transporters affects intracellular pH.

John N. Soltys, M.D., Ph.D.

Assistant Professor

M.D./Ph.D: University of Colorado at Anschutz Medical Campus

Residency: 小蝌蚪APP

Fellowship: University of Oxford, John Radcliffe Hospital

jsoltys@health.southalabama.edu 

Research Interest:  Neuroimmunology, with a focus on multiple sclerosis and paraneoplastic autoimmune brain disease

Mark S. Taylor, Ph.D. 

Professor 

Ph.D.: Basic Medical Sciences, Department of Physiology, 小蝌蚪APP
Postdoctoral Studies: Department of Pharmacology, University of Vermont College of Medicine

mtaylor@southalabama.edu

 

Lab Focus

My laboratory focuses on functional Ca2+ signaling patterns associated with cardiovascular disease and preterm labor. We are particularly interested in elucidating the complex dynamic Ca2+ patterning along the vascular endothelium that preserves cardiovascular homeostasis and becomes disrupted with vascular injury and progressive cardiovascular disease. We also explore phasic Ca2+ signals in the uterus and apply novel approaches to overcome complications associated with dysfunctional labor and delivery. Many of our studies have converged on cooperative ion channels, including inositol trisphosphate receptors (IP3R), Ca2+-activated K+ channels (KCa) and transient receptor potential channels (TRP) that function within distinct cellular domains to generate, tune and direct a wide variety of spatial and temporal Ca2+ signals. Our ultimate goal is to develop targeted therapeutic strategies that preserve, restore or supplement homeostatic patterns and prevent life-threatening disease states. This includes averting the dysfunctional endothelial signaling underlying atherosclerosis, acute respiratory distress, and acute infection as well as exploiting feedback Ca2+ control mechanisms to suppress anomalous uterine contractility in preterm labor.

Our lab employs various approaches including pressure and force myography, molecular biology/immunostaining, and imaging techniques e.g., confocal fluorescence microscopy. We also implement novel high-content approaches for dynamic bio-signal analysis, including custom algorithms designed for autodetection and quantification of dynamic signal parameters. Our laboratory employs various animal models, including conventional and targeted knockout mice, tissue-specific biosensor-expressing mice, partial carotid ligation (low-flow) surgical models, and infection models as well as human vascular and uterine tissues.

 

Lab Team

David S. Weber, Ph.D.

Associate Professor

Ph.D.: Physiology, Medical College of Wisconsin
Postdoctoral Studies: Division of Cardiology, Emory University, Georgia; Department of Physiology, Medical College of Georgia and University of Michigan Medical School

dweber@southalabama.edu

 

Lab Team

Sage Garriss
Graduate Student

Emily Wilson, Ph.D.

Professor

Ph.D: Emory University

Postdoctoral: Vanderbilt University

emilyw@southalabama.edu