Shelly Erickson, PhD (Medicine/Gerontology and Geriatric Medicine)
Our lab’s main objective is to understand mechanisms by which inflammation contributes to brain diseases such as Alzheimer’s.  We are particularly focused on the highly specialized small blood vessels in the brain, which form a blood-brain barrier (BBB) as central mediators of communication between the brain and the body. We hope that our research will ultimately benefit patients by improving the understanding of 1) how signals of inflammation and infection outside of the brain are relayed across the BBB and into the brain, and 2) the short-term and long-term effects of inflammation on brain health.

We are currently using a human induced pluripotent stem cell-derived model of the BBB to understand how inflammatory molecules called chemokines can cross from the bloodstream into the brain, to build improved in vitro models for studying brain inflammation and brain microvascular aging, and to determine how molecules in the bloodstream affect BBB functions in young, healthy subjects and in patients with cognitively normal aging or Alzheimer’s dementia.  We plan to advance our studies into other disease areas such as sepsis, obesity, and diabetes. Accomplishments in these areas have potential for developing personalized medicine diagnostic approaches and better treatments for brain diseases such as Alzheimer’s.

Cecilia Giachelli, PhD (Bioengineering)
My lab is interested in applying stem cell and regenerative medicine strategies to the areas of ectopic calcification, tissue engineering, biomaterials development and biocompatibility.

David Marcinek, PhD (Radiology)
The overriding theme of research in our lab is the interaction between mitochondria and cell stress and its effect on the pathology of chronic disease and aging. Most people learn about mitochondria as kidney bean shaped structures that function as the “Powerhouse of the Cell” by generating chemical energy in the form of ATP. However, mitochondria are actually structurally and functionally dynamic organelles that sit at the nexus between cell energetics, redox biology, and cell signaling. As a result, mitochondrial biology controls many aspects of cell function and plays a critical role in cell, tissue, and organismal responses to acute and chronic stressors. Our interest in muscle satellite cells and regeneration is relatively new and came about as we became interested in the role mitochondrial play in muscle injury and recovery. The two main questions that drive most of our research are:

1) What are the structural changes that lead to increased mitochondrial redox stress with chronic disease?

2) Why does increased mitochondria redox stress translate to cell pathology in some circumstance and adaptive responses in others?

The second question has led us to start collaborations with other ISCRM labs to better understand how changes in mitochondrial function with age and chronic disease alter the ability of muscle satellite cells to respond to stimuli. Answering these questions will improve our understanding the role of mitochondria in disease to help develop targeted interventions to improve quality of life with age and chronic disease.

Ray Monnat, PhD (Pathology, Genome Sciences)
Our research focuses on human RecQ helicase deficiency syndromes such as Werner syndrome; high resolution analyses of DNA replication dynamics; and the engineering of homing endonucleases for targeted gene modification or repair in human and other animal cells.

Peter Rabinovich, MD, PhD (Pathology)
Recent scientific advances have demonstrated that aging is not the immutable process it was once thought to be. A variety of genetic, cellular, and, nutritional interventions not only increase longevity in laboratory organisms, but also dramatically increase the duration of disease-free life. The connection between health and aging is dramatic, as the major causes of human mortality increase exponentially with age, and modest reductions in the rate of aging have dramatic effects on the time of onset of heart disease, cancer, diabetes, etc. There is also a very close connection between aging and regenerative medicine, as we and others believe that that the onset of many diseases of aging is related to a decline in maintenance and repair capacities of cells and organs.

Investigators in the biology of aging at the University of Washington study interventions in the aging process in a variety of organisms, spanning yeast, nematodes, mice and humans. Genetic regulation of lifespan and cellular repair capacities is a special focus of our work. We are excited about the potentials for interaction of work in this field with studies of stem cells and regenerative medicine and believe that the confluence of these fields is a fertile area for rapid advancement.

Jenny Robinson, PhD (Orthopaedics & Sports Medicine and Mechanical Engineering)
Our primary goal is to understand what cues are needed to promote connective tissue (ligament, cartilage, fibrocartilage) regeneration after knee injuries and reduce the onset of osteoarthritis. We have a particular interest on how these cues may differ in male and female athletes. We engineer biomaterial-based environments that mimic native tissue biochemical and mechanical properties to pinpoint specific cues that are required for regeneration of the connective tissues in the knee. We aim to use this knowledge to inform the treatment options for patients with knee injuries to ensure they can get back to performance with reduced or minimal chance for the development of osteoarthritis.

Devin K. Schweppe, PhD (Genome Sciences)
The Schweppe Lab at UW focuses on the study of proteome dynamics in cellular and organismal systems. Using biologically aware mass spectrometric data acquisition we quantify proteins as a readout for diverse cell states with broad interests spanning microbial protein interactions, development, aging, small-molecule binding events, pre-clinical proteomics, and profiling primary tissue samples. Our team builds on the application of sample multiplexing and real-time search to determine how chemicals and drugs drive remodeling of cells on the proteome level. We use these insights to determine desired and undesired consequences of potential therapies in cellular models for expansion to primary mammalian tissues. Along with the methods and technology development focus, the group has worked to build applications and resources to disseminate large-scale proteomics datasets to the research community.

Stuart Shankland, MD, MBA
Kidney disease, which impacts one in nine Americans, leads to loss of certain cell types. Our lab studies both aging and diseases of the glomerulus, the kidney’s filtering units. The glomerular cell called the podocyte is lost in disease, and in the healthy aging kidney. Podocyte loss underlies scarring of the kidney, with loss of kidney function, accompanied by leakage of protein into the urine (proteinuria). However, podocytes are unable to proliferate and thus cannot self-renew. This, their replacement relies on regeneration by neighboring stem/progenitor cells. We have identified that parietal epithelial cells and renin producing cells are podocyte stem/progenitor cells. Ongoing studies in our lab are identifying which small molecules and drugs can increase the regenerative capacity of podocyte stem/progenitor cells to replace podocytes in disease, why regeneration is decreased in the healthy aged kidney and unable to regenerate adequately, and how we can deliver specific therapies to parietal epithelial cells to increase efficiency while minimizing off target effects. The end goal of our studies is to translate these results to the patient with kidney disease by enhancing regeneration in order to restore cell number, integrity and function.