Cell growth, differentiation and development; Cytoskeleton and cell motility; Genomics and proteomics; Molecular and Cellular Biology; Molecular Basis of Disease; Gene Expression; Signal Transduction; Cell Cycle
I am a cell biologist and bioengineer, and my primary research focuses on the rapidly growing area of cell mechanics and mechanotransduction: the role that mechanical forces play in regulating cellular function from healthy to diseased phenotypes. (1) Cardiovascular Biology, Mechanics and Disease: Funding source: American Heart Association (7/1/2018–6/30/2021; PI) Cardiovascular disease (CVD) is the main cause of death globally. Arterial stiffness is associated with many CVD. The molecular mechanisms governing arterial stiffening and the phenotypic changes in vascular smooth muscle cells (VSMCs) associated with the stiffening process are key areas in cardiovascular biology, mechanics and disease. Evidence suggests that arterial stiffening can drive aberrant migration and proliferation of VSMCs within the vessel wall. Yet, the underlying mechanisms regulating vascular stiffening and the molecular changes within VSMCs associated with the stiffening process remain unclear. While medications reduce hypertension, none specifically target pathways directly related to arterial stiffness. The overall goal of work in my lab is to address this gap in our understanding by investigating how changes in arterial stiffness affect VSMC function and fundamentally contribute to the progression of CVD. This study also addresses an important concept in vascular tissue remodeling (the interaction between extracellular matrix stiffness and VSMC behavior). Methodologically, my lab use a novel approach to dissect the molecular mechanism in VSMCs: My lab combines methods for manipulating and measuring tissue and cell stiffness using atomic force microscopy and traction force microscopy for simultaneously modulating substrate stiffness and measuring contraction force by culturing cells on a compliant substrate that mimics in vivo mechanical environments of the VSMCs. (2) Smooth Muscle Cell (and Cancer Cell) Heterogeneity: Highly heterogeneous responses of VSMCs to arterial stiffness or CVD make it difficult to dissect underlying molecular mechanisms. To overcome this, my lab integrates Mechanobiology, Vascular Cell Biology, and Machine Learning to manipulate stiffness and assess responses with unique precision. Machine learning is used to deconvolve inter- and intra-cellular heterogeneity and identify specific subcellular traits that correlate with stiffness and VSMC behavior. My lab also applies Machine Learning approaches to identify specific breast cancer cell behaviors that respond to different stiffness conditions. (3) Optogenetics and Biophotonics in Stem Cell Biology: Funding source: National Science Foundation (8/1/2017–7/31/2020; co-PI) Major breakthroughs in the field of genomics, embryonic stem cell biology, optogenetics and biophotonics are enabling the control and monitoring of biological processes through light. Additional research in my laboratory focuses on developing a nanophotonic platform able to activate/inactivate gene expression and, thus, control stem cell differentiation in neuronal cells, by means of light-controlled protein-protein interactions. More specifically, the light-controlled molecular toggle-switch based on Plant Phytochrome B and transcription factor Pif6 will be utilized to control the nuclear fibroblast growth factor receptor-1, which is a master regulator of stem cell differentiation. Open Positions: The Bae lab is currently accepting graduate students through the Pathology Masters program (or other programs) as well as motivated undergraduates. For Graduate Students: I am looking for one or two graduate (MS) students who understand my research interests, have read my previous publications, and have their own (crazy!!!) ideas as to where my research efforts should be directed. All graduate students are required to complete and submit internationally recognized Journal article(s) before graduation from my lab. A Masters thesis should generate at least one first author publication. For Undergraduate Students: I encourage all UB undergraduates (with GPA 3.0 or higher) to get "hands on" experimental training in the sciences. An undergraduate research project tends to be part of a larger whole, but I make sure to include credit for students work in presentations and publications.
Oncology; Cell Cycle; Cell growth, differentiation and development; Gene Expression; Molecular Basis of Disease; Molecular and Cellular Biology; Signal Transduction; Transcription and Translation
Protein phosphorylation is an essential mechanism by which intercellular signals regulate specific intracellular events. Protein kinases, the enzymes catalyzing protein phosphorylation reactions, represent a major superfamily of genes, collectively representing 2% of the protein coding potential of the human genome. Current projects in Dr. Edelman‘s lab are devoted to the role of protein kinases in prostate and ovarian cancer. These projects utilize a wide range of techniques and involve, collaboration with investigators at Roswell Park Cancer Institute to develop protein kinase-targeted therapies for both types of cancer.
Cardiology; Cardiovascular Disease; Internal Medicine; Apoptosis and cell death; Cell Cycle; Cell growth, differentiation and development; Gene therapy; Stem Cells
I am a researcher with formal training and practice in both general and interventional cardiology. My research expertise is in coronary physiology and physiological studies in large animals with ischemic heart disease. Based on my background, my research is focused on therapeutic approaches to effect cardiac regeneration in large animals with acute and chronic ischemic heart disease. In my laboratory, I use a preclinical porcine model of hibernating myocardium with chronic left anterior descending (LAD) coronary artery occlusion and collateral-dependent myocardium or infarcted myocardium caused by coronary ischemia-reperfusion. I have addressed the problem with several different therapeutic approaches involved in gene therapy, pharmacological and stem cell therapies. We routinely perform physiological studies on these porcine models with quantitative analyses of myocardial morphometry and immune-histochemical analyses. The information we have collected in completed work demonstrates remarkable functional recovery and myocyte regeneration in the adult porcine heart. Intracoronary adenoviral gene transfer with fibroblast growth factor (FGF-5), the HMG-CoA inhibitor pravastatin and intracoronary mesenchymal stem cells (MSCs) all stimulate the proliferation of endogenous cardiac myocytes and, to some extent, generate new myocytes and vessels. Our current work is focused on understanding the regenerative capability of cardiosphere-derived cells (CDCs) originating from heart tissue in acute or chronic ischemic myocardium. The result of this work will play an important role in advancing the care of many patients with acute and chronic ischemic heart disease. In my laboratory, I mentor research fellows through their rotation. Fellows who work in my laboratory have the unique opportunity of being exposed to large animal experimentation and learning skills related to it--in physiology and coronary angiography, as well as computed tomography (CT) and magnetic resonance imaging (MRI) techniques. Under my supervision, fellows also may work on independent projects and learn about cell biology and molecular biology, with the chance to present at international meetings and to publish as an author in international journals.