University of South Alabama

Acute Lung Injury

The Acute Lung Injury focus group seeks to identify novel mechanisms of lung injury and repair, and explore how these mechanisms may be exploited to develop new therapeutics for patient treatment.  Disruption of the endothelial lining in the pulmonary circulation results in widespread alveolar flooding and the development of life-threatening hypoxemia. Historically, research on acute lung injury has focused on understanding the signaling pathways involved in the disruption of the endothelial-epithelial barrier that leads to alveolar flooding. Recovery from acute lung injury requires repair of the disrupted capillary endothelial-alveolar epithelial barrier in the pulmonary microcirculation to re-establish a proper gas exchange unit. The signaling pathways involved in the repair of endothelial and alveolar epithelial cells are distinct from those that lead to the initial injury, and are likely modulated by the local environment. Despite its importance, little is known about the mechanisms involved in pulmonary barrier restoration, and no current therapeutic interventions aim to promote lung repair in affected patients.

Within the CLB, we have a collaborative group of researchers interested in both aspects of acute lung injury, some investigating those factors that initiate acute lung injury (e.g. signaling pathways involved in the disruption of the endothelial-epithelial barrier), and others focused on the mechanisms that promote pulmonary vascular repair.  Members of our research team, and their scientific interests, are listed below. This group employs vertically integrated approaches aimed at dissecting acute lung injury, with expertise ranging from intact animal models and whole lung physiology to cell culture and molecular biology.  We hope you join us!


CLB Faculty
Acute Lung Injury

Alvarez, Diego F., M.D., Ph.D.
Associate Professor
Departments of Internal Medicine and Pharmacology
Acute Lung Injury Group Co-Leader
Phone: (251) 460-6392
Fax: (251) 460-7452
dalvarez@southalabama.edu

Laboratory focus is on the role of progenitor endothelial cells on pulmonary vascular repair following acute lung injury.

Fouty, Brian W., M.D.
Professor
Acute Lung Injury Group Co-Leader
Department of Internal Medicine
Phone: (251) 460-7218
Fax: (251) 460-7452
bfouty@health.southalabama.edu

Laboratory focus is on the role of environmental factors such as glucose and oxygen tension on endothelial function during acute lung injury.

Audia, Jon, Ph.D.
Associate Professor
Department of Microbiology
Phone: (251) 460-6929
Fax: (251) 460-7931
jaudia@southalabama.edu

Laboratory focus is on mechanisms of bacterial virulence, primarily P. aeruginosa and R. prowazekii phospholipases.

Barrington, Robert A., Ph.D.
Assistant Professor
Department of Microbiology
Phone: (251) 461-1718
Fax: (251) 460-7931
rbarrington@southalabama.edu

Laboratory focus is on the role of primary antibodies in the generation of lung injury.

Bauer, Natalie R., Ph.D.
Assistant Professor
Department of Pharmacology
Phone: (251) 461-1567
Fax: (251) 460-7452
nbauer@southalabama.edu

Laboratory focus is on the role of microparticles in acute lung injury.

Brett, Paul J., Ph.D.
Associate Professor
Department of Microbiology and Immunology
Phone:   (251) 414-8179
Fax: (251)-460-7931
pbrett@southalabama.edu

Laboratory focus is on elucidating the molecular mechanisms used by Burkholderia pseudomallei (melioidosis) and Burkholderia mallei (glanders) to subvert host innate immune defenses.

Burtnick, Mary N., Ph.D.
Assistant Professor
Dept of Microbiology and Immunology
Phone 251-460-6204
Fax 251-460-7931
mburtnick@southalabama.edu

Laboratory focus is on understanding the roles of Type III and Type VI secretions systems in the pathogenesis of melioidosis (Burkholderia pseudomallei) and glanders (Burkholderia mallei).

Gillespie, Mark N., Ph.D.
Professor and Chair
Department of Pharmacology
Phone: (251) 460-6497
Fax: (251) 460-6798
mgillesp@southalabama.edu

Laboratory focus is on identifying novel therapies that promote mitochondrial DNA repair in the setting of lung injury.

Parker, James C., Ph.D.
Professor
Department of Physiology
Phone: (251) 460-6826
Fax: (251) 460-6386
jparker@southalabama.edu

Laboratory focus is on the mechanisms involved with ventilator induced lung injury.

Rich, Thomas C., Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6039
Fax: (251) 460-6798
trich@southalabama.edu 

Laboratory focus is on the subcellular compartmentalization of intracellular signals that results in endothelial barrier disruption in the setting of acute lung injury.

Sayner, Sarah, Ph.D.
Assistant Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-6959
Fax: (251) 460-6771
ssayner@southalabama.edu

Laboratory focus is on the environmental signals, such as bicarbonate, that regulate soluble mammalian adenylyl cyclase in control of endothelial cell barrier function.

Stevens, Troy, Ph.D.
Professor
Departments of Internal Medicine and Pharmacology
Director
Center for Lung Biology
Phone: (251) 460-6056
Fax: (251) 460-7452
tstevens@southalabama.edu

Laboratory focus is on the mechanisms inflammatory mediators and bacteria (or bacterial products) utilize to disrupt the endothelial cell barrier in acute lung injury.

Townsley, Mary I., Ph.D.
Associate Dean of Faculty Affairs and Professor
Departments of Physiology and Internal Medicine
Phone: (251) 460-6815
Fax: (251) 460-6386
mtownsley@southalabama.edu

Laboratory focus is on calcium signals that disrupt the endothelial cell barrier, especially in the lung’s microcirculation.

 

Airways and Airway Smooth Muscle

Several laboratories associated with the CLB investigate diverse aspects of development, cell biology and function of the airways and airway smooth muscle.  The faculty members are interested in signaling pathways and molecules that regulate lung development, epithelial fluid transport, smooth muscle contraction, cell migration and cell phenotype.  Relevant disease interests include asthma, cystic fibrosis and bronchiopulmonary dysplasia.  A shared theme of each laboratory is interest in defining cellular and molecular mechanisms of lung pathology that might be exploited in developing novel lung-directed therapies for the diseases of interest.  Expertise exists in a variety of experimental approaches including functional assays of airway secretion and fluid transport, airway smooth muscle mechanics, lung morphology and histology, cell migration, gene expression and RNA-induced silencing.  The broad-based multidisplinary nature of airways research adds to the highly interactive nature of the CLB.

CLB Faculty
Airways and Airway Smooth Muscle

Gerthoffer, William, Ph.D.
Professor and Chair
Department of Biochemistry and Molecular Biology
Airways and Airway Smooth Muscle Leader
Phone: (251) 460-6402
Fax: (251) 460-6850
wgerthoffer@southalabama.edu

Laboratory focus is on signaling pathways controlling contractile and cytoskeletal proteins in airway smooth muscle contraction.  Recent work has explored roles for microRNAs in setting airway smooth muscle phenotype in cells from normal and asthmatic human airways.

Ballard, Stephen, Ph.D.
Professor
Department of Physiology
Phone: (251) 460-6811
Fax: (251) 460-6386
sballard@southalabama.edu

Laboratory focus is on biophysics of ion and water transport, liquid and biomolecule secretion in airways, mucocilliary clearance, and animal models of cystic fibrosis.

Gebb, Sarah, Ph.D.
Assistant Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-414-8050
Fax: (251) 460-6771
sgebb@southalabama.edu

Laboratory focus is on lung development, impact of mitochondrial DNA damage on lung development, cellular and molecular mechanisms of bronchiopulmonary dysplasia.

Pulmonary Endothelial Cell Biology

The Pulmonary Endothelial Cell Biology focus group examines mechanisms that regulate endothelial cell behavior, with a special emphasis on the heterogeneity in structure and function of pulmonary artery, capillary, and vein endothelium.  The pulmonary circulation is the largest circulation in the body; it possesses an enormous surface area, especially within the capillaries.  Pulmonary endothelium is of the continuous subtype, although in recent years, research has begun to reveal the diverse nature of these cells along the vascular axis.  CLB investigators have contributed significantly to our growing awareness of endothelial cell heterogeneity.  Our faculty has examined how pulmonary artery, capillary, and vein endothelial cells uniquely respond to diverse environmental stimuli, including oxygen, carbon dioxide, bicarbonate, various inflammatory mediators, bacteria, viruses and parasites.  We have addressed divergent functions of these cell types in regard to barrier properties, growth, migration, apoptosis, and the production of vasoactive substances such as nitric oxide and prostacyclin.  We have begun to provide complex molecular maps regarding signals that confer endothelial specificity and, further, site-specific endothelial cell specificity.  This is an exciting time in the study of endothelial cell biology.  Come be a part of our program as we divulge basic mechanisms of endothelial cell structure and function, examine how these mechanisms are disrupted or dysfunctional in disease states, and exploit our novel discoveries for development of new therapies to combat vascular disease.


CLB Faculty
Pulmonary Endothelial Cell Biology

Stevens, Troy, Ph.D.
Professor
Departments of Internal Medicine and Pharmacology
Director
Center for Lung Biology
Pulmonary Endothelial Cell Biology Group Leader
Phone: (251) 460-6056
Fax: (251) 460-7452
tstevens@southalabama.edu

Laboratory focus is on the mechanisms of lung endothelial cell heterogeneity.

Alexeyev, Mikhail, Ph.D.
Associate Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-6789
Fax: (251) 460-6771
malexeye@southalabama.edu

Laboratory focus is on developing novel molecular approaches for gene transfection and expression in lung endothelium.

Al-Mehdi, Abu-Bakr, M.D., Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6704
Fax: (251) 460-6798
mehdi@southalabama.edu

Laboratory focus is on mechanisms of mechanotransduction in endothelium.

Alvarez, Diego F., M.D., Ph.D.
Associate Professor
Departments of Internal Medicine and Pharmacology
Phone: (251) 460-6392
Fax: (251-460-7452
dalvarez@southalabama.edu

Laboratory focus is on determining molecular mechanisms that confer progenitor status to resident pulmonary endothelial cells.

Audia, Jon, Ph.D.
Associate Professor
Department of Microbiology
Phone: (251) 460-6929
Fax: (251) 460-7931
jaudia@southalabama.edu

Laboratory focus is on mechanisms of action of bacterial phospholipases, such as the P. aeruginosa and R. prowazekii ExoU.

Balczon, Ron, Ph.D.
Associate Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-6776
Fax: (251) 460-6771
rbalczon@southalabama.edu

Laboratory focus is on identifying mechanisms regulating microtubule dynamics in lung endothelium.

Bauer, Natalie R., Ph.D.
Assistant Professor
Department of Pharmacology
Phone: (251) 461-1567
Fax: (251) 460-7452
nbauer@southalabama.edu

Laboratory focus is on the mechanisms of endothelial cell microparticle release, their molecular composition, and their paracrine role in physiology.

Cioffi, Donna, Ph.D.
Assistant Professor
Department of Biochemistry and Molecular Biology
Phone: (251) 460-6995
Fax: (251) 460-6850
dlcioffi@southalabama.edu

Laboratory focus is on mechanisms by which inflammatory agonists induce endothelial cell cytosolic calcium signals that disrupt the endothelial cell barrier.

Cioffi, Eugene, Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6783
Fax: (251) 460-6798
eacioffi@southalabama.edu

Laboratory focus is on resolving the molecular composition and function of the endothelial cell glycocalyx.

Chinkers, Michael, Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6782
Fax: (251) 460-6798
chinkers@southalabama.edu

Laboratory focus is on the role of natriuretic peptides in differentially regulating endothelial permeability in health and disease.

Fouty, Brian W., M.D.
Professor
Department of Internal Medicine
Phone: (251) 460-7218
Fax: (251) 460-7452
bfouty@health.southalabama.edu

Laboratory focus is on the role of environmental factors such as glucose and oxygen tension on endothelial metabolism and barrier function.

Gillespie, Mark N., Ph.D.
Professor and Chair
Department of Pharmacology
Phone: (251) 460-6497
Fax: (251) 460-6798
mgillesp@southalabama.edu

Laboratory focus is on mechanisms of oxidant injury, especially nuclear and mitochondrial DNA responses to oxidants.

Olson, Jack, Ph.D.
Professor
Department of Pharmacology
Department of Pharmacology
Phone: (251) 461-1367
Fax: (251) 460-6798
jwolson@southalabama.edu

Laboratory focus is on mechanisms underlying endothelial cell proliferation, especially polyamine-dependent cell signals.

Parker, James C., Ph.D.
Professor
Department of Physiology
Phone: (251) 460-6826
Fax: (251) 460-6386
jparker@southalabama.edu

Laboratory focus is on the mechanisms involved in endothelial mechanotransduction.

Rich, Thomas C., Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6039
Fax: (251) 460-6798
trich@southalabama.edu 

Laboratory focus is on the subcellular compartmentalization of intracellular signals that results in endothelial barrier disruption.

Sayner, Sarah, Ph.D.
Assistant Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-6959
Fax: (251) 460-6771
ssayner@southalabama.edu

Laboratory focus is on the environmental signals, such as bicarbonate, that regulate soluble mammalian adenylyl cyclase in control of endothelial cell barrier function.

Townsley, Mary I., Ph.D.
Associate Dean of Faculty Affairs and Professor
Department of Internal Medicine and Physiology
Phone: (251) 460-6815
Fax: (251) 460-6386
mtownsley@southalabama.edu

Laboratory focus is on calcium signals that disrupt the endothelial cell barrier, especially in the lung’s microcirculation.

 

Pulmonary Arterial Hypertension

The Pulmonary Arterial Hypertension (PAH) focus group investigates the cellular mechanisms of pulmonary vasoconstriction and vascular wall remodeling with the goal of identifying more effective therapy for the debilitating and deadly disease. The etiology of PAH can be idiopathic or heritable, or it can develop secondarily to other underlying conditions. Regardless of etiology, the pathogenesis of the pulmonary arterial disease involves dysregulation of numerous vasoactive mediators and cellular signaling pathways that cause sustained pulmonary vasoconstriction, perivascular inflammation, medial and adventitial thickening of proximal pulmonary arteries, fibroproliferative occlusion of distal pulmonary arteries, and in situ thrombosis. The resulting increased pulmonary arterial resistance and stiffness overload the right ventricle and ultimately lead to its failure and the death of PAH patients.  The current clinical management of PAH is hampered by two major impediments. First, the drugs now used are at best only moderately effective. Second, no biomarkers have been identified to provide tracking of either the development of the arteriopathy and right ventricular failure or the response to treatment. Correcting these limitations is imperative to improve quality of life and survival of PAH patients.

Rho kinase (comprising isoforms 1 and 2) is a hub of numerous signal transduction pathways. Whereas basal Rho kinase activity is involved in regulation of normal cellular function, the multifunctional kinase is hyperactivated in various cardiovascular diseases. There is substantial evidence that hyperactive Rho kinase signaling is a key mediator of several of the processes involved in development and progression of PAH. These include endothelial dysfunction, inflammation, vasoconstriction, cell proliferation and migration, fibrosis, and thrombosis. Thus, the central theme of our translational research program is that hyperactivation of Rho kinases not only plays a key role in the pathogenesis of PAH, but also generates circulating biomarkers of the disease severity.  The ultimate goal of our group’s collaborative interaction is to establish new therapeutic strategies to effectively and safely inhibit Rho kinase signaling in the hypertensive pulmonary arteries and failing right ventricle of patients with PAH.  We also seek to determine if circulating, Rho kinase-related microparticles and microRNAs (miRNAs) are sensitive biomarkers of the pulmonary arteriopathy and right ventricular dysfunction, and of the clinical response to Rho kinase-inhibitor therapy. 

Preclinical work is done in our recently characterized late-stage Sugen5416/Hypoxia/Normoxia-exposed rat that shows unusual hemodynamic and pulmonary arteriopathic fidelity to human PAH (Abe et al., Circulation 121: 2747-2754, 2010). This model of occlusive PAH provides a more exacting test of the potential clinical efficacy of new therapeutic candidates than do the traditional chronically hypoxic and monocrotaline-injected models.  Appropriate preclinical findings will be tested in clinical trials in PAH patients receiving conventional therapy in the University of South Alabama Medical Center’s Pulmonary Hypertension Center.   


CLB Faculty
Pulmonary Arterial Hypertension

McMurtry, Ivan, Ph.D.
Professor
Department of Internal Medicine and Pharmacology
Pulmonary Arterial Hypertension Group Leader
Phone: (251) 414-8038
Fax: (251) 460-6798
ifmcmurtry@southalabama.edu

Laboratory focus is on identifying the most effective and safest small-molecule inhibitor and method of delivery to inhibit pulmonary arterial Rho kinase signaling and reverse the pulmonary vasoconstriction and arteriopathy of PAH.

Bauer, Natalie, Ph.D.
Assistant Professor
Department of Pharmacology
Phone: (251) 461-1567
Fax: (251) 460-7452
nbauer@southalabama.edu

Laboratory focus is on the role of cell-derived, circulating microparticles as mediators and biomarkers of pulmonary arterial and right ventricular dysfunction in PAH.

Chinkers, Michael, Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6782 
Fax: (251) 460-6798
chinkers@southalabama.edu

Laboratory focus is on the role of natriuretic peptides in differentially regulating endothelial permeability in health and disease.

Fagan, Karen, M.D.
Professor
Departments of Internal Medicine and Pharmacology
Chief
Pulmonary and Critical Care Medicine
Phone: (251) 471-7914
Fax: (251) 460-7452
kfagan@health.southalabama.edu

Laboratory focus is on the role of integrin signaling in the hyperactivation of pulmonary arterial RhoA/Rho kinase activity.  Clinical focus is on the management of patients with pulmonary hypertension, including those with pulmonary arterial hypertension.

Gerthoffer, William, Ph.D.
Professor and Chair
Department of Biochemistry
Phone: (251) 460-6402
Fax: (251) 460-6850
wgerthoffer@southalabama.edu

Laboratory focus is on development of RhoA/Rho kinase-targeted RNA interference agents, such as siRNAs or miRNAs, that can be used to antagonize the anomalous constriction and occlusive remodeling of pulmonary arteries in PAH.

Oka, Masahiko, M.D., Ph.D.
Assistant Professor
Department of Internal Medicine
Phone: (251) 460-7982
Fax: (251) 460-7452
moka@southalabama.edu

Laboratory focus is on development of angiogenic-homing and cell-penetrating peptides that can be used to selectively deliver Rho kinase inhibitors to hypertensive pulmonary arteries to increase drug efficacy and avoid adverse systemic side effects.

Olson, Jack, Ph.D.
Professor
Department of Pharmacology
Phone: (251) 461-1367
Fax: (251) 460-6798
jwolson@southalabama.edu

Laboratory focus is on mechanisms underlying the aberrant proliferative and survival cell phenotypes that drive the pathogenic arteriopathy of PAH, especially polyamine-dependent signals.

Wagner, Wiltz, Ph.D.
Professor
Department of Pharmacology
Phone: (251) 460-6497
Fax: (251) 460-6798
wwwagner@southalabama.edu

Dr. Wagner has a career-long interest in pulmonary arterial hypertension.  One focus has been on why some species, e.g., sheep, do not raise their pulmonary arterial pressures at high altitude, whereas other species, e.g., cattle develop pulmonary arterial hypertension that can in some cases progress to death.  Yet some cattle are resistant the hypoxia-induced pulmonary hypertension.  The genetic comparisons between and among species is a likely path to understanding and predicting the outcome in human patients.

Nano-Scale Respiratory Biology

The Nano-Scale Respiratory Biology focus group examines nano- and molecular-scale interactions that  govern  cellular responses to the environment. In the last decade we have come to appreciate how seemingly small changes in structural components of pulmonary endothelial and smooth muscle cells markedly impact pulmonary function. Our goal is to understand how such changes ultimately impact our ability to breathe. The projects we pursue are often inspired by observations made in the study of pulmonary disease. For example, P. aeruginosa secretes an enzyme that cleaves a particular sugar in the glycocalyx; ongoing studies are aimed at determining whether this damage to the glycocalyx makes the lung more susceptible to infection. P. aeruginosa also injects exotoxins into epithelial and endothelial cells; exotoxins hijack localized signaling complexes in the host cell, cause changes in cellular structure, and make the lung more susceptible to damage. Compromised endothelial cells release small vesicles that deliver signaling molecules and proteins throughout the vasculature and can trigger system wide inflammatory responses.

Historically it has been difficult to study these processes because the small scale of the events precluded direct measurement. We are active in the development of genetic, biochemical, and imaging approaches to overcome these technical limitations. In particular, we are now able resolve dynamic, inter-molecular events that occur in intracellular and extracellular spaces in vitro and in vivo. Even with technical advances, the mechanisms by which small changes within cells impact pulmonary function remain poorly understood,  making this an area of research ripe with potential. Studies conducted by members of this group are inherently multidisciplinary, with biologists, clinicians, chemists, and engineers working in concert. This offers an unique and collaborative training environment for students, faculty, and fellows in multifaceted studies of pulmonary physiology and pathophysiology.

CLB Faculty
Nano-scale Respiratory Biology

Alexeyev, Mikhail, Ph.D.
Associate Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-6789
Fax: (251) 460-6771
malexeye@southalabama.edu

Laboratory focus is on developing novel molecular approaches for gene transfection and expression in lung endothelium.

Al-Mehdi, Abu-Bakr, M.D., Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6704
Fax: (251) 460-6798
mehdi@southalabama.edu

Laboratory focus is on mechanisms of mechanotransduction in endothelium.

Alvarez, Diego F., M.D., Ph.D.
Associate Professor
Departments of Internal Medicine and Pharmacology
Phone: (251) 460-6392
Fax: (251-460-7452
dalvarez@southalabama.edu

Laboratory focus is on determining molecular mechanisms that confer progenitor status to resident pulmonary endothelial cells.
 
Audia, Jon, Ph.D.
Associate Professor
Department of Microbiology
Phone: (251) 460-6929
Fax: (251) 460-7931
jaudia@southalabama.edu

Laboratory focus is on mechanisms of action of bacterial phospholipases, such as the P. aeruginosa and R. prowazekii ExoU.

Balczon, Ron, Ph.D.
Associate Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-6776
Fax: (251) 460-6771
rbalczon@southalabama.edu

Laboratory focus is on identifying mechanisms regulating microtubule dynamics in lung endothelium.

Bauer, Natalie R., Ph.D.
Assistant Professor
Department of Pharmacology
Phone: (251) 461-1567
Fax: (251) 460-7452
nbauer@southalabama.edu

Laboratory focus is on the mechanisms of endothelial cell microparticle release, their molecular composition, and their paracrine role in physiology.

Cioffi, Donna, Ph.D.
Assistant Professor
Department of Biochemistry and Molecular Biology
Phone: (251) 460-6995
Fax: (251) 460-6850
dlcioffi@southalabama.edu

Laboratory focus is on mechanisms by which inflammatory agonists induce endothelial cell cytosolic calcium signals that disrupt the endothelial cell barrier.

Cioffi, Eugene, Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6783
Fax: (251) 460-6798
eacioffi@southalabama.edu

Laboratory focus is on resolving the molecular composition and function of the endothelial cell glycocalyx.

Gerthoffer, William, Ph.D.
Professor and Chair
Department of Biochemistry
Phone: (251) 460-6402
Fax: (251) 460-6850
wgerthoffer@southalabama.edu

Laboratory focus is on development of RhoA/Rho kinase-targeted RNA interference agents, such as siRNAs or miRNAs, that can be used to antagonize the anomalous constriction and occlusive remodeling of pulmonary arteries in PAH.

Gillespie, Mark N., Ph.D.
Professor and Chair
Department of Pharmacology
Phone: (251) 460-6497
Fax: (251) 460-6798
mgillesp@southalabama.edu

Laboratory focus is on mechanisms of oxidant injury, especially nuclear and mitochondrial DNA responses to oxidants.

Leavesley, Silas, Ph.D.
Assistant Professor
Department of Chemical and Biomolecular Engineering
Phone: (251) 460-6160
Fax: (251) 461-1485
leavesley@southalabama.edu

Laboratory focus is on the development and application of in vitro and in vivo imaging techniques.

Rich, Thomas C., Ph.D.
Associate Professor
Department of Pharmacology
Phone: (251) 460-6039
Fax: (251) 460-6798
trich@southalabama.edu 

Laboratory focus is on the subcellular compartmentalization of intracellular signals that result in endothelial barrier disruption.

Sayner, Sarah, Ph.D.
Assistant Professor
Department of Cell Biology and Neuroscience
Phone: (251) 460-6959
Fax: (251) 460-6771
ssayner@southalabama.edu

Laboratory focus is on the environmental signals, such as bicarbonate, that regulate soluble mammalian adenylyl cyclase in control of endothelial cell barrier function.
 

 

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