ArticleJournal of biomechanics2019
Primary human chondrocytes respond to compression with phosphoproteomic signatures that include microtubule activation.
Article in Journal of biomechanics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Compressive stress-driven mechanosignaling in chondrocytes: From molecular mechanism to scaffold engineering and translational opportunities.Materials today. Bio · 2026Review
- Development of the mechanoresponsive pericellular matrix of chondrons.Science advances · 2025Article
- Phlpp1 alters the murine chondrocyte phospho-proteome during endochondral bone formation.Bone · 2024Article
- From polarity to pathology: Decoding the role of cell orientation in osteoarthritis.Journal of orthopaedic translation · 2024Review
- Hippo-PKCζ-NFκB signaling axis: A druggable modulator of chondrocyte responses to mechanical stress.iScience · 2024Article
- Pericellular Matrix Formation and Atomic Force Microscopy of Single Primary Human Chondrocytes Cultured in Alginate Microgels.Advanced biology · 2024Article
- An overview of substrate stiffness guided cellular response and its applications in tissue regeneration.Bioactive materials · 2022Review
- Metabolomic Profiling and Mechanotransduction of Single Chondrocytes Encapsulated in Alginate Microgels.Cells · 2022Article
- MicroRNA‑186‑5p downregulation inhibits osteoarthritis development by targeting MAPK1.Molecular medicine reports · 2021Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Chondrocytes are responsible for maintaining the cartilage that helps joints bear load and move smoothly. These cells typically respond to physiological compression with pathways consistent with matrix synthesis, and chondrocyte mechanotransduction is essential for homeostasis. In osteoarthritis (OA), chondrocyte mechanotransduction appears to be dysregulated, yet the mechanisms remain poorly understood. The objective of this study is to document the phosphoproteomic responses of primary osteoarthritic chondrocytes to physiological sinusoidal compression. We show that OA chondrocytes respond to physiological compression by first activating proteins consistent with cytoskeletal remodeling and decreased transcription, and then later activating proteins for transcription. These results show that several microtubule-related proteins respond to compression. Our results demonstrate that compression is a relevant physiological stimulus for osteoarthritic chondrocytes. Future analyses may build on these results to find differences in compression-induced phosphoproteins between normal and OA cells that lead to druggable targets to restore homeostasis to diseased joints.
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Registered trials
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