Katherine Wood, PhD
Dr. Wood’s current research in the Straub lab is focused on determining the role of a novel reduction-oxidation (redox) regulation mechanism — the CyB5R3-dependent reduction of sGC — in the control of NO sensitivity in vascular smooth muscle cells (VSMCs) and its impact on SCD vasculopathy. SCD vasculopathy is multifactorial and the pathogenesis remains incompletely understood, although both clinical and experimental evidence concludes that reduced NO bioavailability and/or responsiveness are contributing factors. Dr. Wood researches the impact of this signaling pathway on the development of cardiopulmonary vasculopathy in the humanized transgenic sickle cell mouse (Townes) and chimeras transplanted into tamoxifen-inducible Cre-Lox smooth muscle specific CyB5R3 knock-out and loss of function CyB5R3 T117S polymorphic variants. The overall goal of the research is to test personalized and precision medicine approaches to improve the health of individuals with SCD-associated pulmonary hypertension. Considering the defining role of sGC in NO signaling and the fact that the oxidation state of sGC may predict responses to new classes of sGC activator and stimulator medications, is research aims to significantly impact our understanding of biology, precision therapeutics (right drug for the right patient) and pharmacogenetics (polymorphism based drug selection).
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Scott Hahn, MS
Research Technician, Microvascular and Hypertension Core
Scott earned both his bachelors and masters degrees in Kinesiology from Kansas State University. His research experience prior to joining the Straub lab in 2014 included the study of necrotizing enterocolitis, angiogenesis, cancer, obesity and diabetes. His main focus in the lab is the use of myography to study vascular reactivity in disease states and genetic modifications. Additionally, he performs a multitude of in vivo procedures in mice to study real time blood pressure and heart rate, heart hemodynamics, and various other surgical procedures.
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Megan focuses on understanding the role of cytochrome b 5 reductase 3 (cyb5R3) in nitric oxide (NO) signaling in smooth muscle cells and endothelial cells. Cyb5R3 has dual functions in the vascular wall; 1) regulating NO diffusion from endothelial cells to smooth muscle cells by reducing hemoglobin in the myoendothelial junction and 2) sensitizing soluble guanylate cyclase to NO in smooth muscle cells by reducing it to its ferrous state. Megan employs a number of biochemical and in vitro cell culture based techniques to address the functional roles of Cyb5R3.
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Graduate Student, Interdisciplinary Biomedical Graduate Program
There are many different isoforms of the forkhead box (FOX) transcription factors found throughout the body and while many of them are essential for proper tissue differentiation and development, there are a number of FOX transcription factors that have been recently implicated as promoters of longevity and cellular survival. One such protein, FOXO3a has been shown to help regulate cellular quiescence, and downregulation of FOXO3a activity is often seen in cancer. In addition, FOXO3a is commonly upregulated in most centenarians in humans, and its homologs, daf-16 and dFOXO in C. elegans and Drosophila melanogaster have been shown to be associated with increased longevity. Joe is interested in the regulatory mechanisms by which FOXO3a may be contributing to better survival outcomes and the methods by which it is able to regulate the proliferation of vascular cell types
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Graduate Student, Physician Scientist Training Program
Macrophages are monocyte-derived innate immune cells that display an incredibly diverse array of functions, ranging from roles in fetal development to the immune response to pathogens. During times of infection or tissue damage, macrophages are activated and release of a collection of products, including cytokines; the freely-diffusible biogas, nitric oxide (NO); and reactive oxygen species (ROS). These products, along with other macrophage-specific functions, are crucial for the initiation and perpetuation of the inflammatory response. Our lab has shown that CYB5R3 is a critical regulator of NO release in the vasculature, however, the role of CYB5R3 in immune cell function remains unexplored. Using a variety of in vitro and in vivo methods, Jake is interested in characterizing the function of CYB5R3 in macrophages, with a focus on its potential role in the inflammatory response.
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Student Research Assistant | AHA SURP recipient, 2016
Our lab has shown Cytochrome B5 Reductase 3 (CyB5R3) plays a major role in vascular biology, although it’s importance in the cardiomyocyte function is not yet understood. In preliminary pharmacological studies, CytB5R3 small molecule inhibitor treatments resulted in major cardiac remodeling and impaired hemodynamic function. Using a cardiac specific knockout animal developed in our lab, Nolan is investigating the molecular basis for this pathology. In doing so, Nolan has shown CyB5R3 is critical for cardiomyocyte survival and investigates the diminished metabolic capacity caused by the loss of CyB5R3. His current work seeks to elucidate the necessity of CyB5R3 in maintenance of proper metabolic and mitochondrial function in the heart through various cell, animal, and human models.
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Previous Lab Members
Roger Alvarez, DO, MPH
Assistant Professor, Pulmonary & Critical Care Medicine, Miller School of Medicine, University of Miami
Anh Tram Nguyen, PhD
Research Scientist, University of Virginia
Md Mizanur Rahaman, PhD
Assistant Professor, Tohoku University, Japan
Graduate Student, Molecular Pharmacology Graduate Program, University of Pittsburgh