Microscale frictional strains determine chondrocyte fate in loaded cartilage
| Autor: | Edward D. Bonnevie, Lena R. Bartell, Naveen Jasty, Lawrence J. Bonassar, Lisa A. Fortier, Itai Cohen, M.L. Delco |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
Cartilage
Articular 0301 basic medicine Programmed cell death Friction 0206 medical engineering Biomedical Engineering Biophysics 02 engineering and technology Mitochondrion Article Chondrocyte Weight-Bearing 03 medical and health sciences Chondrocytes Materials Testing Synovial Fluid medicine Shear stress Animals Humans Synovial fluid Orthopedics and Sports Medicine Chemistry Cartilage Rehabilitation 020601 biomedical engineering Biomechanical Phenomena Cell biology 030104 developmental biology medicine.anatomical_structure Arthritis therapy Apoptosis Stress Mechanical |
| Zdroj: | Journal of Biomechanics. 74:72-78 |
| ISSN: | 0021-9290 |
| DOI: | 10.1016/j.jbiomech.2018.04.020 |
| Popis: | Mounting evidence suggests that altered lubricant levels within synovial fluid have acute biological consequences on chondrocyte homeostasis. While these responses have been connected to increased friction, the mechanisms behind this response remain unknown. Here, we combine a frictional bioreactor with confocal elastography and image-based cellular assays to establish the link between cartilage friction, microscale shear strain, and acute, adverse cellular responses. Our incorporation of cell-scale strain measurements reveals that elevated friction generates high shear strains localized near the tissue surface, and that these elevated strains are closely associated with mitochondrial dysfunction, apoptosis, and cell death. Collectively, our data establish two pathways by which chondrocytes negatively respond to friction: an immediate necrotic response and a longer term pathway involving mitochondrial dysfunction and apoptosis. Specifically, in the surface region, where shear strains can exceed 0.07, cells are predisposed to acute death; however, below this surface region, cells exhibit a pathway consistent with apoptosis in a manner predicted by local shear strains. These data reveal a mechanism through which cellular damage in cartilage arises from compromised lubrication and show that in addition to boundary lubricants, there are opportunities upstream of apoptosis to preserve chondrocyte health in arthritis therapy. |
| Databáze: | OpenAIRE |
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