Please use this identifier to cite or link to this item: http://hdl.handle.net/1880/51436
Title: The effect of compressive loading magnitude on in situ chondrocyte calcium signaling
Authors: Herzog, Walter
Madden, Ryan M.J.
Han, Sang-Kuy
Keywords: Articular cartilage;chondrocyte;calcium signaling;mechanobiology;mechanotransduction
Issue Date: May-2014
Publisher: Biomech Model Mechanobiol
Biomechanics and modeling in mechanobiology
Citation: Madden, R. M., Han, S. K., & Herzog, W. (2015). The effect of compressive loading magnitude on in situ chondrocyte calcium signaling. Biomechanics and modeling in mechanobiology, 14(1), 135-142.
Abstract: Chondrocyte metabolism is stimulated by deformation and is associated with structural changes in the cartilage extracellular matrix (ECM), suggesting that these cells are involved in maintaining tissue health and integrity. Calcium signaling is an initial step in chondrocyte mechanotransduction that has been linked tomany cellular processes. Previous studies using isolated chondrocytes proposed loading magnitude as an important factor regulating this response. However, calcium signaling in the intact cartilage differs compared to isolated cells. The purpose of this study was to investigate the effect of loading magnitude on chondrocyte calcium signaling in intact cartilage. We hypothesized that the percentage of cells exhibiting at least one calcium signal increases with increasing load. Fully intact rabbit femoral condyle and patellar bone/cartilage samples were incubated in calcium-sensitive dyes and imaged continuously under compressive loads of 10–40% strain. Calcium signaling was primarily associated with the dynamic loading phase and greatly increased beyond a threshold deformation of about 10%nominal tissue strain. There was a trend toward more cells exhibiting calcium signaling as loading magnitude increased (p =0.133). These results provide novel information toward identifying mechanisms underlying calcium-dependent signaling pathways related to cartilage homeostasis and possibly the onset and progression of osteoarthritis.
URI: http://hdl.handle.net/1880/51436
Appears in Collections:Herzog, Walter

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