Graduate Student, Biomedical Engineering
Osteoporosis and hypertension are both highly prevalent diseases and comorbidities of aging. Recent clinical studies suggest that these diseases may contribute to one another through common inflammatory and immune pathways. More specifically, the effect of hypertension on the bone marrow microenvironment may skew hematopoietic stem cells toward myeloid cells and osteoclastic phenotypes. Preliminary results from our lab suggest that increasing the stretch experienced by bone marrow-derived endothelial cells increases the transcription and production of recombinant macrophage-colony stimulating factor (MCSF). This factor is an integral part of both myeloid differentiation and osteoclastogenesis. We hypothesize that the increase in MCSF production by endothelial cells in the bone marrow microenvironment, encourages osteoclast formation. This increases one’s risk for bone reabsorption and, inevitably, osteoporosis. Therefore, this research aims to better understand the mechanisms by which stretch influences M-CSF production and enables osteoclast formation. In doing so, one may be able to identify new strategies for counteracting lowered bone strength by inhibiting mechanisms of hypertension.