Research Interest: Cardiovascular Biology
| 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. |
| Leiderman, Karin WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
I am a mathematical biologist interested in the biochemical and biophysical aspects of blood clotting and emergent behavior in biological fluid-structure interaction problems. I especially love mathematical modeling, where creativity, biological knowledge, and mathematical insight meet. My goal is to use mathematical and computational modeling as a tool to learn something new about a biological system, not just to simply match model output to experimental data. My research paradigm includes an integration of mathematical and experimental approaches, together with statistical analyses and inference, to determine mechanisms underlying complex biological phenomena. This paradigm culminates in the contextualization of my findings to both the mathematical and biological communities. My research program is focused mainly on studying the influence of biochemical and biophysical mechanisms on blood coagulation, clot formation, and bleeding. |
| Luu, Anh |
PHD PROGRAM RESEARCH INTEREST |
|
| Edwards, Whitney PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Our lab aims to identify the fundamental molecular mechanisms underlying heart development and congenital heart disease. Our multifaceted approach includes primary cardiac cell culture, genetic mouse models, biochemical/molecular studies, and transcriptomics. Additionally, we employ proteomics-based methods to investigate 1) protein expression dynamics, 2) protein interaction networks, and 3) post-translational modifications (PTMs) in heart development. Current research projects focus on investigating the function of two essential PTMs in cardiogenesis: protein prenylation and palmitoylation. |
| Kim, Boa WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Endothelial cells, which comprise the innermost wall of all blood vessels, are involved in a broad range of metabolic and cardiovascular diseases that represent a global challenge with high morbidity. Endothelial cell metabolism is an active process, and altered endothelial metabolism drive disease progression. The research in my lab focuses on the molecular mechanisms of endothelial cell metabolism and how they affect cardiovascular and metabolic diseases. |
| Maeda, Nobuyo PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Overall goal of our research is to gain better knowledge of gene-gene and gene-environment interactions in common cardiovascular conditions in humans. We have been modifying mouse genome in such a way that resulting mice can model quantitative variations of a specific gene product that occur in human population. With these mice, we explore causes, mechanisms, and nutritional treatments of cardiovascular complications resulted from common conditions such as diabetes, lung infections, and pregnancy-associated hypertension. Current focus is on the oxidative stress and effects of vitamin B12 as antioxidant and beyond. |
| Wirka, Robert WEBSITE |
PHD PROGRAM RESEARCH INTEREST |
Our lab uses human genetics to identify new mechanisms driving coronary artery disease (CAD). Starting with findings from genome-wide association studies (GWAS) of CAD, we identify the causal gene at a given locus, study the effect of this gene on cellular and vessel wall biology, and finally determine the molecular pathways by which this gene influences CAD risk. Within this framework, we use complex genetic mouse models and human vascular samples, single-cell transcriptomics/epigenomics and high-throughput CRISPR perturbations, as well as traditional molecular biology techniques. |
| Aleman, Maria WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
The broad goal of our research is to understand basic mechanisms regulating erythropoiesis (red blood cell differentiation and maturation). Our current work focuses on a family of dual functional proteins (poly C binding proteins) which both regulate RNA processing and chaperone iron within cells. Using biochemical, cellular, and in vivo models we explore the cross talk between iron trafficking and RNA regulation mediated by poly C binding proteins and how these activities are modulated by disease. |
| Rau, Christoph WEBSITE PUBLICATIONS |
PHD PROGRAM RESEARCH INTEREST |
Heart failure is an increasingly prevalent cause of death world-wide, but the genetic and epigenetic underpinnings of this disease remain poorly understood. Our laboratory is interested in combining in vitro, in vivo and computational techniques to identify novel markers and predictors of a failing heart. In particular, we leverage mouse populations to perform systems-level analyses with a focus on co-expression network modeling and DNA methylation, following up in primary cell culture and CRISPR-engineered mouse lines to validate our candidate genes and identify potential molecular mechanisms of disease progression and amelioration. |
| Jensen, Brian WEBSITE |
PHD PROGRAM RESEARCH INTEREST |
Our lab uses cell culture and animal models to define the mechanisms that lead to heart failure and to identify novel approaches to its treatment. We are particularly interested in the roles of inflammation and cardiomyocyte metabolism in the pathobiology of the failing heart. Ongoing projects focus on (1) the cardioprotective role of the alpha-1A adrenergic receptor; (2) transcriptional regulation by the nuclear receptor ROR-alpha; (3) cardiotoxicity of antineoplastic kinase inhibitors. |