Phone: (979) 862-9134
My laboratory has been engaged in multiple areas of NIH-funded musculoskeletal research since 1996. We were the first to identify the non-steroidal gonadal inhibin hormones in regulating the hypothalamic-pituitary-gonadal-skeletal axis in mice, and the role of changes in inhibins that signal the onset of menopause to the onset of increasing bone turnover. In addition, we demonstrated the anabolic effect of continual Inhibin exposure in normal mice and in bone repair. Our cellular focus on Inhibins and the related factor, Activin A revealed that Activin A suppresses local bone resorption through suppression of osteoclast formation, motility and survival. Another research interest has focused on understanding the mechanisms involved in musculoskeletal (MSK) aging, disuse, fracture healing and restoration of the MSK system by reambulation and exercise. Our metastatic bone disease efforts have been aimed at identifying biomarkers that predict breast cancer bone metastasis and demonstrating their usefulness as targets for therapeutic development. We have also developed techniques that better quantify the host reactive bone formation response to S. aureus infection in the development of osteomyelitis. Finally, we are greatly interested in improving the low bone mass that we were the first to identify in both humans with Down Syndrome (DS) and in mouse models of DS as a low bone turnover disease. We are now actively testing molecules to increase bone mass in mouse models of Down Syndrome. Collectively, our multifaceted interest in the skeleton have utilized rodent models of distraction osteogenesis, gonadectomy, hindlimb suspension, and transgenic models, as well as the analytical methods of ex vivo microCT, histomorphometry and ex vivo bone marrow cultures. We hope to expand these studies in the near future to larger animal models that better replicate the processes of human bone remodeling.
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