The effect of compressive loading magnitude on in situ chondrocyte calcium signaling

• Published in: Biomechanics and modeling in mechanobiology Vol. 14; no. 1; pp. 135 - 142
• Main Authors: Madden, Ryan M. J., Han, Sang-Kuy, Herzog, Walter
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.01.2015; Springer Nature B.V
• Subjects: Animals; Biological and Medical Physics; Biomechanics; Biomedical Engineering and Bioengineering; Biophysics; Bones; Calcium; Calcium - metabolism; Calcium Signaling - physiology; Cartilage; Cartilage, Articular - cytology; Cartilage, Articular - physiology; Cellular; Chondrocytes - physiology; Compressive Strength - physiology; Deformation; Engineering; In Vitro Techniques; Loads (forces); Mechanotransduction, Cellular - physiology; Original Paper; Osteoarthritis; Rabbits; Signal transduction; Space life sciences; Strain; Stress, Mechanical; Texts; Theoretical and Applied Mechanics; Calcium signaling; Mechanotransduction; Articular cartilage; Chondrocyte; Mechanobiology
• ISSN: 1617-7959; 1617-7940
• DOI: 10.1007/s10237-014-0594-4

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 to many 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.