The long-term goal of the Antonetti laboratory is to contribute to the development of novel treatments to prevent or reverse the debilitating loss of vision from diabetes. Our laboratory is specifically interested in the tight junction complex in specialized regions of the vasculature that help to create the blood-brain and blood-retinal barrier. The tight junctions that connect the endothelial cells in the brain and retina are needed for normal neural function and may be compromised in a variety of disease states. Diabetic retinopathy is the leading cause of visual loss in working age adults and ischaracterized by increased vascular permeability, leading to edema, or fluid accumulation, in the retina. Our laboratory works to understand the cellular and molecular basis for this change in vascular permeability by exploring the changes in the tight junction complex that controls the blood-retinal barrier. This research has led to the development of novel therapeutic approaches to treat these diseases.
The Hershenson laboratory studies cellular and molecular mechanisms underlying chronic airways diseases such as asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis and bronchopulmonary dysplasia. We are currently focusing on 3 major areas of study: (i) Pathogenesis of rhinovirus-induced exacerbations of chronic airways diseases including asthma and COPD, (ii) Role of mesenchymal stem cells in lung injury and repair, and (iii) Signal transduction mechanisms underlying airway smooth muscle cell hypertrophy and differentiation in asthma.
The Moore laboratory is interested in two main areas. The first is understanding the pathogenesis of fibrotic lung diseases. The second is studying lung host defense, particularly following stem cell transplantation. In our fibrosis work, we are currently working to understand how the matricellular protein periostin can contribute to the development and progression of fibrotic disease by exploring the influence of periostin on alveolar epithelial cells and fibroblasts. In our host defense work, we are working to understand how prostaglandin dysregulation alters innate immne function and how transforming growth factor beta regulates adaptive immune function. In these models we study both bacterial and viral infections.
Effective tissue immunity requires effective clearance of noxious agents coupled with timely resolution of inflammation to allow tissue repair and regeneration, ability to remember the initial transgressor, and then prompt, apt responsiveness to subsequent re-encounter. All these processes need finely regulated, intimate crosstalk between the epithelial cells, the noxious stimuli (microbes, allergens, cancer cells), innate immune cells (like macrophages, neutrophils, etc.), and adaptive immune cells (like T cells). The Shenoy Lab of Barrier Immunobiology (SLOBI) is interested in understanding the extent of- and mechanisms underlying- how this intercellular crosstalk to- and from- lung epithelial cells remodels lung immunity to optimize immune resistance (noxious stimuli clearance) while ensuring/impeding tissue resilience (lung function) during health and disease.
My research focuses on the pathobiology of pulmonary fibrosis with the goal of defining new therapeutic strategies for these difficult to treat diseases. In this regard, I have been specifically interested in determining the link between epithelial injury and the induction of lung scarring. I have also been working to define the mechanism by which the profibrotic mediator plasminogen activator inhibitor-1 (PAI-1) promotes fibrogenesis.
The central theme of the Spence lab is to understand how the endoderm and its associated organs develop, with a focus on intestine and lung development. The lab uses human pluripotent stem cells to generate 3-dimensional tissues in the tissue culture incubator. The lab also uses model organisms to explore the molecular mechanisms that control embryonic development. By understanding how the embryo develops, we gain insights into how abnormal development can lead to congenital disease, or how developmental regulators are involved in regeneration, injury repair or disease in the adult.
The Wang laboratory focuses on the molecules that participate in neuronal injury, with a specific interest in genetic causes of stroke and molecular mechanisms of neuroprotection. Specifically, we investigate (1) Pathogenesis of CADASIL / Regulation of Notch 3 signaling, (2) Nuclear receptor signaling in stroke, (3) Effects of stroke on sleep and circadian rhythms, and (4) BMP regulation of dendritogenesis.
Dr. Wang is NOT accepting fellows for Summer 2023.
Richard C. Schneider Research Professor, Neurosurgery
Dr. Xi's research interests are mechanisms of brain injury after hemorrhagic stroke and preconditioning-induced neuroprotection. His work has demonstrated that iron contributes to brain edema formation and neurodegeneration following intracerebral hemorrhage and has resulted in a deferoxamine clinical trial for intracerebral hemorrhage.
The Zochowska laboratory focuses on biology of blood brain barrier and cerebral microvasculature. We are studying the structure and function of protein complexes in the blood brain barrier (BBB) using molecular and cell biologic approaches. We are particularly interested in mechanism of the BBB/junctional complex “opening” during neuroinflammatory process as well as the alteration of the junctional complex during the process of the vascular “aging”. Other projects in our laboratory are related to the study mechanisms and factors involved in the tight junction assembly in cerebral microvasculature during the process of angiogenesis and Blood brain barrier recovery.