Faculty Research Interests
Michael Buszczak, Ph.D.
We seek to understand how mRNA translation and chromatin organization help to maintain the balance between stem cell self-renewal and differentiation in vivo.
Thomas Carroll, Ph.D.
The Carroll lab is interested in the mechanisms underlying stem cell renewal and differentiation in the kidney. Much of our research focuses on how the ultimate fate of progenitor cells is affected by their microenvironment.
Ondine Cleaver, Ph.D.
Our lab aims to elucidate the molecular events required for cells to proliferate and take on their specialized functions within tissues such as the pancreas and blood vessels. Understanding these principles will help us to characterize genes that may be required to reactivate these processes during tissue regeneration, as well as to identify molecular lesions that underlie human birth defects and disease.
Jim Collins, Ph.D.
Schistosomes are parasitic flatworms that cause significant disease and disability in more than 200 million of the world’s poorest people. Using a variety of functional genomic approaches we seek to understand fundamental aspects of schistosome biology, including the biology of somatic and reproductive stem cells.
Rhonda Bassel-Duby, Ph.D.
We are interested in understanding the molecular mechanisms that regulate striated muscle (skeletal muscle and heart) during regeneration in response to injury and disease. We study molecular factors that control satellite cells, which are skeletal muscle stem cells. We are also defining factors involved in reprogramming fibroblasts to cardiac cells to repair the heart after injury.
Fred Grinnell, Ph.D.
Research in my laboratory focuses on the biomechanics of connective tissue repair and the pathobiological features that influence healing of human burn and chronic skin wounds. My studies concern not only the research itself, but also the nature of scientific practice underlying research and the bioethical challenges of carrying out research with humans.
Robert Hammer, Ph.D.
We are involved in mouse embryonic stem cell biology and genetic manipulation of the rodent genome.
Joseph Hill, M.D., Ph.D.
Dr. Hill’s research group strives to decipher mechanisms of structural, functional, and electrical remodeling in heart disease with an eye toward therapeutic intervention. Our work is disease-oriented, focusing on load-induced ventricular hypertrophy, ischemia/reperfusion injury, and diabetic cardiomyopathy. Specific areas of emphasis include HDAC-dependent control of cardiac plasticity, cardiomyocyte autophagy, metabolism, and FoxO-driven transcriptional events.
Jenny Hsieh, Ph.D.
Contrary to accepted dogma, human beings retain the ability to grow new nerve cells throughout life. The Hsieh lab studies the cellular and molecular mechanisms of neurogenesis to understand how stem cells become mature, functioning nerve cells. We also study how aberrant neurogenesis contributes to seizure formation, an unwarranted side effect of neuroregenerative strategies.
Rueyling Lin, Ph.D.
The major goal of my lab is to understand the molecular mechanisms underlying cell fate specification and cell polarity during animal development. In particular, we focus on how different signaling pathways (Wnt, MAP kinase, and Notch) intersect to regulate these processes. Re-establishment of appropriate cell and tissue polarity is a key step toward successful regeneration. By understanding how these signaling pathways regulate cell polarity and cell fate specification, our studies will contribute to improved and controlled regeneration.
Ning Liu, Ph.D.
We are interested in the mechanism of heart repair and regeneration after myocardial injury. We study the functions of a unique population of cardiac progenitor cells in cardiac regeneration under normal and diseased conditions. Understanding the mechanisms of cardiac regeneration is an essential step toward improving the regenerative capacity of the adult heart.
Lawrence Lum, Ph.D.
The Lum lab studies cellular communication systems that coordinate cell fate decision-making in metazoans. Several signaling molecules that govern adult tissue homeostasis, including Wnt and Hedgehog, provide the investigative framework for regenerative medicine agendas.
Raymond MacDonald, Ph.D.
Our interests are the molecular mechanisms that specify and maintain cell-type identity, explain the plasticity of cellular identity in adulthood, and may be manipulated for tissue regeneration.
Pradeep Mammen, M.D.
The Mammen Laboratory seeks to investigate how alterations in the metabolic and redox states of myogenic progenitor cells can modulate the proliferative and differentiative capacities of these cells. Ultimately, the ability to selectively regulate the metabolic and redox states of cardiac and myogenic progenitor cells may provide opportunities for the development of novel therapeutic approaches for the treatment of patients with advanced heart failure and/or muscular dystrophy.
Joshua Mendell, M.D., Ph.D.
The Mendell laboratory investigates the regulation and functions of microRNAs and other noncoding RNAs in mammals. We are particularly interested in the roles of these transcripts in normal physiologic processes, including wound healing and tissue regeneration, and in diseases such as cancer.
Sean Morrison, Ph.D.
My lab studies the mechanisms that regulate stem cell self-renewal in the hematopoietic and nervous systems and the ways in which those mechanisms are hijacked by developmentally related cancers to enable neoplastic proliferation.
Nikhil Munshi, M.D., Ph.D.
Our lab seeks to understand the molecular mechanisms by which lineage commitment is achieved in the cardiac conduction system. We believe that such fundamental insight will guide future efforts to regenerate the conduction system and restore normal cardiac rhythm in patients suffering from arrhythmias.
James Richardson, D.V.M., Ph.D.
My lab studies the pathology of genetically engineered mice from prenatal stages to late adulthood.
Hesham Sadek, M.D., Ph.D.
We have recently made a number of fundamental observations outlining the transient regenerative potential of the newborn mammalian heart and the role of cardiomyocyte proliferation in heart regeneration. We are currently focusing on identifying mechanisms of cardiomyocyte cell cycle regulation and developing strategies to reawaken the regenerative potential of the adult heart.
Jay Schneider, M.D., Ph.D.
The Schneider lab focuses on novel strategies for heart repair after injury or disease, using small molecules like isoxazole, which was identified in a stem-cell-based screen of the UT Southwestern chemical compound library, or large molecules like alginate, a seaweed-derived polysaccharide biopolymer that mediates a process of hydrogel heart repair known as "seaweed myocardial regeleration." Dr. Schneider is also the Hub PI for the NHLBI Progenitor Cell Biology Consortium, a U01-funded national network of stem/progenitor cell biologists and regenerative medicine experts.
Ann Word, M.D.
The Word Lab seeks to define the molecular, matricellular, and hormonal machinery that controls regeneration and repair of the injured vaginal wall after childbirth or surgery. We use mouse models of pelvic organ prolapse and animal models of injury to optimize matrix regeneration of the female pelvic floor.
Chun-Li Zhang, Ph.D.
Our laboratory is interested in understanding the genetic and epigenetic regulation of neurogenesis in adult brain and spinal cord. Through modulating and inducing endogenous neurogenesis, we hope to empower the central nervous system to repair itself following post-traumatic injuries or degeneration. A second line of research uses reprogrammed human motor neurons as a therapeutic approach for human neural degenerative diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy.
Hao Zhu, M.D.
We aim to define the genetic and cellular machinery that controls regenerative capacity and injury resistance in the liver. With this knowledge, we have developed mouse models that possess enhanced mammalian regeneration in the liver and in other organs. Ultimately, we will ask how such improvements in mammalian regeneration influences cancer formation.