Noah Mahnke
Pronouns: He/Him
Research Mentor(s): Yuji Mishina
Research Mentor School/College/Department: Biological and Material Sciences / Dentistry
Program:
Authors: Noah Mahnke, Jay More, Jackson Albright, Yuji Mishina
Session: Session 4: 1:40 pm – 2:30 pm
Poster: 103
Abstract
Bone homeostasis is significantly impacted by both growth factor signaling and mechanical loading. Bone Morphogenetic Protein (BMP) signaling is crucial for bone development and maintenance, with BMPs commonly referred to as bone inducers. However, it has been shown that disruption of BMP signaling in osteoblasts can lead to increased bone mass by suppressing osteoclastogenesis, contrary to the traditional understanding of BMPs as bone inducers. Furthermore, mechanical loading has been observed to increase bone mass in mice with osteoblast-specific knockout (cKO) of Bmpr1a, the gene encoding type 1 receptors of BMPs, compared to control mice. The skeleton is an active organ that continuously undergoes remodeling in response to mechanical stress, with osteoblasts laying down bone and osteoclasts absorbing bone. Evidence suggests that mechanical stress promotes osteoblast proliferation. Osteocytes, derived from osteoblasts, are considered to be the primary sensors of mechanical loading. There is a consensus that osteocyte morphology is linked to its ability to sense mechanical stimuli, with round osteocytes being more sensitive than flat osteocytes. Additionally, BMP signaling influences the maturation process of osteocytes. The mechanisms underlying the amplified effect of mechanical loading on bone mass in Bmpr1a cKO mice are not fully understood. This study aims to elucidate how BMP signaling interacts with mechanical loading to influence osteocyte activity. To achieve this, we will utilize transmission electron microscopy (TEM) images to analyze osteocyte morphology in exercised and unexercised Bmpr1a cKO and control mice.
