Courtney M. Karner

University of Texas Southwestern Medical Center, Charles and Jane Pak Center for Mineral Metabolism and Clinical Research, Department of Internal Medicine

Dr. Karner is broadly trained in mouse genetics and embryology as well as bone and kidney biology. The Karner lab strives to understand the molecular underpinnings of cell fate specification and differentiation using bone development and homeostasis in the mouse as a model system. To do this, they focus primarily on the skeletal stem cell (SSC), a multipotent progenitor that gives rise to bone-forming osteoblasts. On the most basic level, osteoblasts are secretory cells responsible for producing and secreting the Collagen Type 1 rich extracellular matrix that comprises bone. Protein synthesis and secretion are demanding both from an energetic and biosynthetic standpoint requiring copious amounts of amino acids, ATP, and other metabolites. As such, the Karner lab focuses on osteoblast metabolism, namely what nutrients do osteoblasts require and how do they utilize them to generate the biomass to sustain the high rates of protein synthesis associated with proliferation, differentiation, and bone formation. Ultimately, the long-term goal of the Karner lab is to leverage this basic metabolic knowledge to rationally design therapeutic strategies to increase osteoblast differentiation and bone formation in patients with low bone mass disorders.

Elizabeth (Beth) Rendina-Ruedy

Vanderbilt University Medical Center, Division of Clinical Pharmacology, Medicine & Vanderbilt University, Molecular Physiology and Biophysics

Dr. Rendina-Ruedy’s unique training and research experience are deeply rooted in the basic science of bone biology with an emphasis on nutritional biochemistry. The Rendina-Ruedy Lab is focused on developing a comprehensive understanding of how metabolic pathways impact bone health. Bone is an incredibly dynamic tissue that undergoes continuous remodeling involving bone-resorbing osteoclasts, bone-forming osteoblasts, and mechano-sensing osteocytes. Due to the high energetic demands of this process targeting metabolic pathways in bone cells is an incredibly provocative tool that can be applied to combat various conditions that lead to increased fracture incidence (i.e., post-menopausal osteoporosis, type 2 diabetes mellitus, and age-related osteoporosis). As such, the Rendina-Ruedy lab has ongoing projects aimed at understanding how bone cells, and cells within the bone marrow niche, store, mobilize, and utilize various metabolic substrates.  In addition to understanding how these metabolic pathways impact bone health in a cell-autonomous manner, our lab is particularly interested in how alterations in bone cell bioenergetics modulate whole-body metabolism.