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Allen, Matthew R., PhD

Our laboratory studies the tissue-level mechanisms responsible for musculoskeletal integrity in health and disease. We utilize numerous in vivo model systems to understand how disease and pharmaceutical intervention influence bone structure, cellular activity, tissue-level properties (such as mineralization, microdamage, collagen, hydration), and biomechanical properties. We study diseases/conditions such as osteoporosis, diabetes, osteoporosis imperfecta, chronic kidney disease, disuse, and aging using techniques such as imaging (CT, DXA, X-ray), histology (static and dynamic histomorphometry, microdamage), and mechanical testing (bending, compression, fatigue, reference point indentation). Our laboratory is funded by the NIH, NASA/NSBRI, and industry.

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Bellido, Teresita M., PhD

Our laboratory investigates the mechanisms of signal transduction among and within bone cells, with particular emphasis on the biology of osteocytes. We employ in vitro, ex vivo and in vivo models to study how hormones and mechanical force act on bone cells and affect their function and life span. Current projects investigate the regulation of the osteocyte-derived genes by PTH; the mechanisms by which PTH, mechanical stimulation, and canonical Wnt signaling regulate bone homeostasis through actions on osteocytes; and interventions that counteract the deleterious effects of glucocorticoid excess on bone and muscle. Collaborative projects investigate the function of connexin43 in bone; the role of estrogen receptor beta in osteocytes for mechanobiology; the regulation of phosphate metabolism and FGF23 action in bone and kidney; and the role of osteocytes in cancer in bone and in the response of bone to radiation. We receive funding from the NIH, VA, DoD, and NOF. 

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Bidwell, Joseph P., PhD

The research mission of our lab is the improvement of therapies for restoring bone lost to osteoporosis or other diseases. We have identified a gene that represses the efficacy of medications used to add new bone to the osteoporotic skeleton. We are using state-of-the-art molecular, cellular, and animal model approaches to design strategies for blocking the action of this gene, i.e. inhibiting the bone inhibitor. The DOD and Eli Lilly currently funds the ongoing work in our laboratory.

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Bonewald, Lynda, PhD

Dr. Bonewald’s research focuses on the biology and function of the osteocyte.  At present there are two major focus areas, the first is on crosstalk between osteocyte and muscle.  Muscle secretes factors that maintain osteocyte viability and function and conversely osteocytes produce factors that support myogenesis and muscle function.  These factors are being identified and their functions characterized.  A second focus of the lab is the role of the osteocyte in calcium homeostasis under calcium demanding conditions such as during pregnancy.  The mechanisms by which osteocytes can remove and replace calcium in their microenvironment is being examined. Trainees can learn osteocyte and muscle cell culture, isolation of primary osteocytes and muscle satellite cells, muscle contractility,  application of fluid flow shear stress, mitochondrial imaging, loading and unloading of transgenic animals, in addition to standard molecular approaches and analyses.

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Burr, David B., PhD

 The primary area of research emphasis is to evaluate the effects of pharmacologic agents used to treat osteoporosis on properties associated with quality of the bone matrix, specifically, the accumulation and repair of microdamage, changes in mineralization and alterations to the collagenous matrix. We have been investigating matrix effects of bisphosphonates and other anti-remodeling agents for many years using canine models. In the past several years, we have begun to investigate changes in matrix in Type 2 diabetes using similar approaches in the ZDSD and ZDF rat models of diabetes.  My laboratory is equipped to characterize histological and dynamic histomorphometric features of different tissues, and to utilize bone density (BMD) and imaging techniques (µCT, pQCT) to analyze tissues in animal models.  This has allowed me to bring mechanical concepts to the study of biological form, function and physiological processes at various length scales.

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Deane, Andrew, PhD

As a paleoanthropologist, my research addresses questions related to ape and human evolution. Specifically, I am interested in the functional relationships between the mechanical loading associated with dietary and locomotor adaptations and hard and soft tissue anatomy, and what these relationships might reveal about the paleoebiology and evolution of fossil apes and early humans. The more accurate our interpretations of fossil ape and early human locomotor adaptations and diet, the greater the potential for that information to contribute answers to research questions about why these taxa evolved, what made them successful in some cases, and extinct in others, and the connection between diet and locomotion and the origins of the lineages of living apes and humans.

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Jesus Delgado-Calle, Ph.D.

Osteocytes are the most abundant cells in bone and are considered as master regulators of bone homeostasis. My research focuses on the mechanisms by which osteocytes contribute to generate a microenvironment that is conducive to tumor progression, bone destruction and muscle weakness in multiple myeloma disease. Current projects investigate the effects of genetic and pharmacological inhibition of osteocyte-derived factors (i.e Sclerostin, Rankl) in tumor growth and multiple myeloma-induced bone fragility and muscle weakness; the role of bidirectional Notch signaling between MM cells and osteocytes in multiple myeloma disease; and the effects of Aplidin (a novel anti-tumor drug that targets eEF1A2), alone or in combination with other anti-tumor drugs, on bone cells and tumor progression. I also collaborate in studies examining the role of osteocytes in multiple myeloma-induced bone pain; the regulation of the skeletal actions of parathyroid hormone; and the deleterious effects that glucocorticoids have in the skeleton. These studies are funded by NIH (Roodman and Bellido), the American society of Hematology (Delgado-Calle), and PharmaMar S.A. (Bellido and Delgado-Calle).

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McNulty, Margaret A., PhD

The McNulty Lab is involved in both basic science and educational research.
Basic science research interests revolve around bone and joint pathology. The McNulty lab uses both advanced imaging (e.g. micro-computed tomography) and histological techniques to evaluate changes in bones and joints secondary to various diseases and treatments. Current work involves projects focused on two specific areas: characterizing and understanding the mechanisms of arthritic changes secondary to chikungunya virus and evaluating the impact of bisphosphonate administration on the equine skeleton. 

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Plotkin, Lilian I., PhD

My research project focuses on the role of connexins in the transduction of signals induced by hormonal, pharmacotherapeutic and mechanical stimuli in osteoblasts and osteocytes. For this, we utilize in vitro techniques including tissue culture, analysis of protein expression by Western blotting and of gene expression by real time PCR. In addition, we perform ex vivo cultures of bone cells isolated from mice treated with pharmacologic and hormonal agents, and from genetically modified mice. Lastly, we have generated genetically modified mice, and characterized their bone phenotype using in vivo and ex vivo imaging, gene expression techniques and histomorphometric analysis. As a result of our studies, we demonstrated that bisphosphonates, agents widely used to treat osteoporosis, prevent osteocyte and osteoblast apoptosis via a novel mechanism that involves opening of connexin43 hemichannel and activation of intracellular signaling molecules. My lab has unveiled a new role of connexin43 on the maintenance of osteocyte viability and in the composition of the bone matrix. Moreover, we have linked for the first time changes on the molecular composition of the cells in bone with cell death and deficient material properties.

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Robling, Alexander G., PhD

Mechanical loading of the skeleton from daily activities determines to a large extent how the skeleton develops. Without proper exercise and loading activities, the skeleton will develop with insufficient strength, and osteoporotic fractures will eventually occur. Our laboratory seeks to discover the molecular mechanisms by which bone tissue senses mechanical loading. We study how several signal transduction pathways affect bone accumulation, and how cellular activity is altered by mechanical stimulation. To do this, we investigate bone cell proliferation, differentiation, and apoptosis, after mechanical loading in mice harboring various mutations in the Wnt/Akt/Bmp signaling pathways. We also study the role of these pathways in disuse, using several in vivo models of disuse osteoporosis.

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Organ, Jason M., PhD

The overall aim of my laboratory research is to understand the biological mechanisms of mechanical adaptation of bone and muscle. The current focus is on the relationship between bone and muscle mechanics at the whole-organ level, and how adaptations of tissue-level morphology influence whole-organ function. This is being investigated through these broadly-defined studies: 

  1. Enhancing bone and muscle quality and function in the context of osteogenesis imperfeca and chronic kidney disease
  2. Effect of altered mechanical loading environment on the mechanical properties of the growing and adult musculoskeletal system
  3. In vivo assessments of bone and muscle structure and function
  4. Mammalian functional anatomy and evolution

Techniques we use include high-resolution imaging, histomorphometry, muscle electrophysiology, and bone mechanical testing. Our laboratory is funded by the NIH and IUSM/Showalter Research Trust.

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Sankar, Uma, PhD

Our laboratory uses global and conditional knockout mouse models, biochemical, molecular biology and cell biology techniques as well as pharmacological inhibitors to investigate the mechanisms by which members of the Calcium/calmodulin dependent protein kinase (CaMK) signaling cascade, CaMKK2 along with its downstream kinases AMPK, CaMKI and CaMKIV; regulate the fate and function of bone marrow-derived mesenchymal stem cells, osteoblasts and osteoclasts.  We are currently pursuing in vivo translational studies investigating CaMKK2 inhibition as a bone anabolic strategy in accelerating fracture healing and combating age and cancer-associated osteoporosis.  Further, CaMKK2 is over-expressed in prostate cancer and recent studies identify it to be a direct target of androgen receptor. We are interested in identifying the effects of CaMKK2 inhibition in prostate cancer-associated bone metastasis as well as establishing the identity of its downstream targets in prostate cancer as well as bone cells. Our laboratory is funded by the American Cancer Society, Department of Defense and the NIH. 

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Department of Anatomy & Cell Biology | IU School of Medicine | 635 Barnhill Drive, MS 5035 | Indianapolis, IN 46202 | (317) 274-7494