Primary Research Focus
Global mortality rates are led by cardiac disease, yet many of its causes are unknown. A long-term interest of the Faustino Lab is the identification and characterization of novel regulators involved in the development and progression of cardiac pathology.
Specifically, we are interested in understanding cell nucleus dynamics that underlie the progression and severity of electrical and muscle disorders of the heart. Greater understanding of these processes will advance the field in innovative directions that support our ultimate goal to improve strategies to address heart disease.
Our work uses several platforms that model cardiac disease processes to help us address our scientific interest.
Spontaneous and induced models of heart failure allow us to study structural and functional changes in the heart in a physiological setting, while a variety of animal and human cell-based platforms allow us to examine mechanistic changes at the subcellular level.
In addition, we use epigenomic, transcriptomic, and proteomic based approaches paired with bioinformatic analyses to understand the molecular networks, or systems biology processes, underlying cardiac pathology.
The immediate objectives of these approaches are designed to help us elucidate non-sarcomeric and non-channelopathy etiologies that account for idiopathic cardiac pathologies, with the ultimate goal of identifying novel targets that can be used to treat heart disease.
About the Faustino Lab
Lab Projects and News
Stem Cell Modeling of Cardiac Disorders
A powerful method to study cardiac disorders is through stem cells. We can introduce experimental and clinically reported genetic variants into specific genes in stem cells, then differentiate and examine the structure and function of cardiac cells that result from the modified stem cells. Then we can begin to discern the underlying cellular mechanisms that may be involved in the development of heart disease.
Cardiac Disease and Nuclear Envelope Biology
The nucleus is the main repository of a cell’s DNA, and access to this genetic information is regulated by the nuclear envelope. Disruption of normal nuclear envelope function often underlies cardiac disease. To have a better understanding of how this plays a role in cardiopathology, we study if and how specific proteins of the nuclear envelope are affected in healthy and failing hearts.
Mapping Cardiac Molecular Networks
We use a combination of next-generation sequencing techniques and bioinformatic analyses to map the molecular networks that impart specific hierarchical functions to cardiac cells. As these networks can be disrupted in cardiac disease, understanding which molecules are involved and how they interact can offer insights into which genes or proteins may be targeted to treat cardiac pathology.
Meet the Faustino Lab Team
Claudia Preston, MD
Staff Scientist (2016)
Dr. Claudia Preston is studying the relationship of Nup155 and serine and arginine rich splicing factor 2 (SRSF2), and its role in cardiac development. She designs and conducts experiments; analyzes and interprets data; prepares scientific writing and illustrations; and mentors graduate and undergraduate students. She completed medical school in Hidalgo, Mexico. She conducted postdoctoral research in the cancer immunology and immunotherapy and cardio-gerontology laboratories at Mayo Clinic.
Tyler has been with the Faustino Lab since 2017. He is responsible for the maintenance of cells lines and performing basic science experiments. In particular, he works on projects investigating cardiac precursor development from human induced pluripotent stem cells as well as investigating mechanisms for enucleation as it relates to erythrogenesis. He has a Bachelor of Science and Master of Science in medical biology from the University of South Dakota.
Emily Storm, MS
Emily is currently enrolled as a graduate student in the MD/PhD program within the Sanford School of Medicine at the University of South Dakota. Her graduate research will investigate the molecular relationship of NUP155 and HDAC4, and how this interaction affects chromatic access and dynamics in cellular and physiological models of cardiac development.