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• W3065486149 abstract "Inflammation triggers degradation of intervertebral disc extracellular matrix (ECM), a hallmark of disc degeneration that contributes to back pain. Mechanosensitive nucleus pulposus cells are responsible for ECM production, yet the impact of a proinflammatory microenvironment on cell mechanobiology is unknown. Using gain- and loss-of-function approaches, we show that tumor necrosis factor-α (TNFα)-induced inflammation alters cell morphology and biophysical properties (circularity, contractility, cell stiffness, and hydraulic permeability) in a mechanism dependent on actomyosin contractility in a three-dimensional (3D) culture. We found that RhoA activation rescued cells from TNFα-induced mechanobiological disruption. Using a novel explant-in-hydrogel culture system, we demonstrate that nuclear factor kappa-B nuclear translocation and transcription are mechanosensitive, and its downstream effects on ECM degradation are regulated by actomyosin contractility. Results define a scaling relationship between circularity, contractility, and hydraulic permeability that is conserved from healthy to inflammatory microenvironments and is indicative of cell mechanobiological control across scales in 3D." @default.
• W3065486149 created "2020-08-24" @default.
• W3065486149 creator A5076843217 @default.
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• W3065486149 date "2020-08-21" @default.
• W3065486149 modified "2023-09-29" @default.
• W3065486149 title "Actomyosin contractility confers mechanoprotection against TNFα-induced disruption of the intervertebral disc" @default.
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• W3065486149 doi "https://doi.org/10.1126/sciadv.aba2368" @default.
• W3065486149 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7438088" @default.
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