USA Department of Physiology & Cell Biology Faculty
Troy Stevens, Ph.D.
Lenoir Louise Locke Chair of Physiology and Cell Biology
Ph.D.: Colorado State University
Post-doctoral: University of Colorado
Phone: (251) 460-6056
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.
Mikhail Alexeyev, Ph.D.
Postdoctoral Studies: Texas Heart Institute
Ph.D.: National Academy of Sciences of Ukraine, Kiev
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’s 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 “humanized” mice could be used as a novel, faithful platform for modeling human mitochondrial diseases using patients’ blood as a source of mutant mtDNA.
Natalie R. Gassman, Ph.D.
B.A.: Chemistry, Michigan State University
Ph.D.: Physical Chemistry, University of California at Los Angeles
Postdoc: Physics, Wake Forest University
Postdoc: Cancer Biology, Wake Forest University
Phone: (251) 445-8430
The focus of my lab is two-fold. First, we want to understand how environmental exposure to endocrine disruptors and other oxidizing chemicals induce DNA damage and alter DNA repair pathways to influence the development and progression of cancer. Then, we want to use our knowledge of DNA damage and altered DNA repair pathways to improve tumor classification and targeting of cancer therapeutics for breast and ovarian cancers. We have developed novel strategies to characterize DNA damage and changes in DNA repair pathways within cells and tissues. With our methods, we can better understand how exposures injury cells and lead to cancer, and we can better identify molecular targets for cancer treatment.
Ji Young Lee, M.D., Ph.D.
Medical Degree: Pusan National University, Pusan, South Korea
Residency: Lincoln Medical and Mental Health Center, Bronx, NY
Fellowship: University of South Alabama College of Medicine
Postdoctoral Studies: University of South Alabama College of Medicine
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.
Mike T. Lin, Ph.D.
B.S.: Biochemistry, University of British Columbia
Ph.D.: Physiology, Loma Linda University
Postdoc: Oregon Health and Science University
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.
Amy R. Nelson, Ph.D.
Ph.D.: University of Alabama at Birmingham
Postdoctoral Studies: University of Southern California
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’s 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’s disease.
Sarah Sayner, Ph.D.
Ph.D.: University of South Alabama
Postdoctoral Studies: University of Cambridge England and University of South Alabama
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.
David S. Weber, Ph.D.
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
Xiangming Zha, Ph.D.
B.Sc.: Shanghai JiaoTong University, 1991
M.Sc.: Shanghai Brain Research Institute, 1994
Ph.D.: University of Iowa, 2000
Postdoc: University of Iowa, with Drs. Steven Green and Michale Dailey, and University of Iowa and HHMI, with Dr. Michael J. Welsh
Phone: (251) 460 6769
Fax: (251) 460 6771
We have been investigating how a reduced brain pH contributes to the etiology of various neurological diseases. The main focus is on proton-mediated signaling through acid-sensitive ion channels and G protein coupled receptors. We use a combination of in vitro and in vivo models in mice to examine how altering these receptors impact neuron function, animal behavior, and ischemic brain injury.
Gerd Heusch, Prof. Dr. med., Dr. h.c.
Direktor des Institutes für Pathophysiologie
Zentrum für Innere Medizin
Thomas Krieg, Dr. med.
Clinical Pharmacology Unit
University of Cambridge
Cambridge CB2 2QQ, UK
Derek Yellon, Ph.D., D.Sc.
Department of Academic & Clinical Cardiology
University College Hospital London, England
Marilyn P. Merker, Ph.D.
Medical College of Wisconsin
Dept. Veterans Affairs
VAMC Milwaukee, WI
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