Research Interest: Stem Cells
| Name | PhD Program | Research Interest | Publications |
|---|---|---|
| Azizoglu, Berfin WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our lab studies body-wide control of organ growth and regeneration. The mammalian body is reticulated by blood vessels and neurons. How these networks communicate with organ cells to orchestrate local and body-wide decisions is obscure. We study this question with a focus on the mouse liver, the uniquely regenerative visceral organ. Current projects in the lab include 1-researching the role of a novel vascular progenitor network in liver regeneration, 2-determining the mechanisms of injury perception by liver innervation, and 3-in vitro assembly of reticulated, responsive liver tissue. |
| Laidman, Ashlyn |
PHD PROGRAM RESEARCH INTEREST |
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| Perrault, Laura |
PHD PROGRAM RESEARCH INTEREST |
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| Chen, Gang WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
We use cutting edge technology to study pathogenesis of human pulmonary diseases including cystic fibrosis, Job’s syndrome, idiopathic pulmonary fibrosis by both human specimens, mouse genetic models, with a goal of finding the therapies. Recently, we developed a serial of lung epithelial-lineage tracing systems, providing the powerful tools for identify mechanisms of lung disease involved in post-acute sequelae SARS-CoV-2 infection, also known as “long COVID”, in collaboration with Dr. Ralph Baric’s Lab at UNC-CH. |
| McCauley, Heather WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The McCauley Lab is interested in how the food we eat changes our physiology. Rare, nutrient sensing cells in the intestine called enteroendocrine cells secrete hormones in response to environmental cues that orchestrate systemic metabolism. How these cells regulate their neighbors in the gut is not well understood. We use mouse models which lack enteroendocrine cells and human pluripotent stem cell derived intestinal organoids to discover new roles for these master metabolic cells in the regulation of intestinal physiology and function. Enteroendocrine cells are dysregulated in inflammatory bowel disease, type 2 diabetes, and obesity, and loss of enteroendocrine cells results in malabsorptive diarrhea with poor survival. Our research has the potential to improve human health for a wide segment of the global population. |
| Good, Misty WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The Good Laboratory is focused on the cellular and molecular mechanisms involved in the pathogenesis of a devastating intestinal disease primarily affecting premature infants called necrotizing enterocolitis (NEC). The long-term goal of the Good Lab is to understand the signaling pathways regulating the uncontrolled immune response in NEC and how these responses can be prevented through dietary modifications or targeted intestinal epithelial therapies. Her basic and translational research utilizes a bench-to-bedside approach with multiple cutting-edge techniques. In her pre-clinical studies, their team utilizes a humanized neonatal mouse model of NEC to understand the signaling pathways and immune cell responses involved in NEC development. Specifically, the laboratory interrogates ways to modulate the immune response, epithelial cell and stem cell regeneration as well as early microbial colonization during NEC. In the clinical component of her research program, Dr. Good leads a large multi-center NEC biorepository for the dedicated pursuit of molecular indicators of disease and to gain greater pathophysiologic insights during NEC in humans. Dr. Good also developed a premature infant intestine-on-a-chip model to study NEC and provide a personalized medicine approach to test new therapeutics. Her laboratory is currently funded with multiple NIH R01 grants and has previously received K08 and R03 funding as well as awards from the March of Dimes, the Gerber Foundation and the NEC Society. |
| Diekman, Brian WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
A major focus of the Diekman lab is to develop new strategies to limit age-related osteoarthritis (OA). The lab uses genetically-engineered mouse models to investigate the development of cellular senescence in joint tissues with physiologic aging. One goal of this work is to determine whether “senolytic” compounds that induce selective apoptosis in senescent cells will mitigate OA development. Our group has also developed genome-editing protocols for primary human chondrocytes to produce single-cell derived colonies with homozygous knockout of target genes. We are using engineered tissues from these cells to dissect the mechanism of genes implicated in OA development by genome-wide association studies, as well as coupling these technologies to high throughput screening approaches for OA drug discovery. |
| Hingtgen, Shawn WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Imagine a naturally intelligent therapy that can seek out and destroy cancer cells like no other available treatment. In the Hingtgen Lab, we are harnessing Nobel Prize-winning advancements to create a new type of anti-cancer treatment: personalized stem cell-based therapies. We use a patient’s own skin sample and morph it into cells that chase down and kill cancer. We take advantage of a little-known aspect of stem cells- they can home in on cancer by picking up a signal through receptors on the cell surface. All the while, the therapeutic stem cells are pumping out potent anti-cancer drugs that selectively kill any cancer cell nearby while leaving the healthy brain unharmed. Our initial studies focused on aggressive brain cancers, however we quickly expanded our testing to a variety of cancer types. Working at the interface of basic science and human patient testing, our ultimate goal is to translate this novel approach into the clinical setting where it can re-define treatment for cancers that currently have no effective treatment options. |
| Williams, Scott E. WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Interest areas: Developmental Biology, Cell Biology, Cancer Biology, Stem Cells, Genetics PhD programs: Pathobiology & Translational Sciences, Genetics & Molecular Biology, Cell Biology & Physiology, Oral Biology, Biology Tissue development and homeostasis depend on the precise coordination of self-renewal and differentiation programs. A critical point of regulation of this balance is at the level of cell division. In the Williams lab, we are interested in stratified epithelial development, stem cells, and cancer, with a particular interest in how oriented cell divisions contribute to these processes. Asymmetric cell divisions maintain a stable pool of stem cells that can be used to sustain tissue growth, or mobilized in response to injury. However, dysregulation of this machinery can lead to cancer, particularly in epithelia where tissue turnover is rapid and continuous. Using the mouse epidermis and oral epithelia as model systems, we utilize cell biological, developmental and genetic approaches to study the molecular control of oriented cell divisions and mitotic spindle positioning, and how division orientation impacts cell fate choices in development, homeostasis, injury, and disease. |
| Gupton, Stephanie WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
During cell shape change and motility, a dynamic cytoskeleton produces the force to initiate plasma membrane protrusion, while vesicle trafficking supplies phospholipids and membrane proteins to the expanding plasma membrane. Extracellular cues activate intracellular signaling pathways to elicit specific cell shape changes and motility responses through coordinated cytoskeletal dynamics and vesicle trafficking. In my lab we are investigating the role of two ubiquitin ligases, TRIM9 and TRIM67, in the cell shape changes that occur during neuronal development. We utilize a variety techniques including high resolution live cell microscopy, gene disruption, mouse models, and biochemistry to understand the complex coordination of cytoskeletal dynamics and membrane trafficking driving neuronal shape change and growth cone motility in primary neurons. |