Maxwell Lemkau
Pronouns: he, him
Research Mentor(s): Yuji Mishina
Co-Presenter: Albright, Jackson
Research Mentor School/College/Department: Biological and Material Sciences / Dentistry
Presentation Date: April 20
Presentation Type: Poster
Session: Session 4 – 2:40pm – 3:30 pm
Room: League Ballroom
Authors: Maxwell Lemkau, Jackson Albright, Honghao Zhang, Yuji Mishina
Presenter: 34
Abstract
Deviations from normal bone homeostasis are characteristic of poor bone health. Pathologic low bone mass is regarded as osteoporosis. More than 200 million people suffer from osteoporosis worldwide. Growth factor signaling and mechanical loading are two especially important factors that affect bone homeostasis. It is well established that Bone Morphogenetic Protein (BMP) signaling plays critical roles in bone development and homeostasis, and BMPs are generally known as bone inducers. Interestingly and contradictory to the knowledge of BMPs as bone inducers, we have found that disruption of BMP signaling in osteoblasts results in increased bone mass through osteoclastogenesis suppression (1). What’s more, mechanical loading increases bone mass in mice with an osteoblast-specific knockout (cKO) of Bmpr1a, the gene that encodes type 1 receptors of BMPs, compared to control mice (2). Osteocytes detect mechanical loading to regulate bone remodeling. It is also believed that BMP signaling influences osteocyte maturation (3) and that osteocyte morphology is related to its ability to sense mechanical loading (4). This study aims to gain a better understanding of the mechanisms behind the increased effect of mechanical loading on bone mass in Bmpr1a cKO. Specifically, how does BMP signaling interact in conjunction with mechanical loading to change osteocyte activity? To achieve this, we used morphology of osteocytes as a proxy for their activity and analyzed TEM images of osteocytes in exercised and unexercised Bmpr1a cKO and control mice. We hypothesize that if BMP signaling and mechanical loading indeed cooperatively regulate osteocyte activity, osteocyte morphology of Bmpr1a cKO exercised mice will be rounder (i.e., more mechanosensitive) than osteocytes of controls. We expect that round osteocyte morphology in Bmpr1a cKO exercised mice. These results would lead us to argue that BMP signaling is implicated in the negative regulation of osteocyte mechanosensing activity.
Biomedical Sciences, Interdisciplinary, Natural/Life Sciences
