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• W3020227834 abstract "Purpose: Molecular mechanisms of OA onset and progression are still poorly understood. Standard in vitro models as well as animal models still face limitations concerning human predictability. Consequently, therapeutic approaches to restore compromised cartilage tissue or decelerate disease progression of OA have not been identified yet. Methods: As advanced in vitro model, organs-on-a-chip are considered an enabling technology that provide a more physiologic cellular microenvironment for recapitulation of organotypic tissue function in vitro. Likewise, organs-on-a-chip can be used to recreate pathophysiological cues including biochemical as well as biomechanical stimuli that trigger onset of disease phenotypes in human-derived in vitro tissues. Pathological changes concerning human OA joints include articular cartilage degradation, thickening of the subchondral bone, formation of osteophytes, synovial inflammation and hypertrophic joint capsule. We propose a human synovium-on-a-chip that enables mechanistic studies concerning direct and indirect cell-cell interaction during OA onset and progression. The integration of non-invasive scattering biosensors enables time-resolved analysis of tissue-level architectural changes during inflammatory remodeling of synovial tissue. Results: On the one hand, we demonstrate that the integration of complex human synovial organoid cultures from primary fibroblast-like synoviocytes in an organ-on-a-chip provides reproducible and reliable information on how systemic inflammatory stress factors affect synovial tissue architecture within two to three days of organoid culture during upregulation of IL-6 and cadherin-11 mediated synovial network remodelling. On the other hand, organ-on-a-chip technology is used for defined nutrient gradients in cartilage organoids to emulate the characteristics of native cartilage including expression of cartilage matrix proteins aggrecan (Acan), collagen type 2 (Col2), and a marker for chondrogenic differentiation (Sox9). Additionally, the organoids were subjected to inflammatory cytokines including tumor necrosis factor TNF-α and interleukin IL-1β to trigger arthritis phenotype with upregulated inflammatory mediators such as aggrecanase (ADAMTS5), interleukin (IL-6), matrixmetalloproteinases (MMP-1, MMP-3, and MMP-13), as well as ColX. A small screening study for clinical inflammatory medication (one JAK-inhibitor and triamcinolone corticosteroid) was performed to demonstrate how the proposed joint-on-a-chip platform can be used to screen for drug efficacy on individual patient-derived samples. Conclusions: To conclude, organs-on-a-chip can provide a technology platform to generate new insights into molecular and biophysical cues at the cellular microenvironment that may govern onset and progression of OA in vitro for both synovial as well as chondral tissue." @default.
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• W3020227834 date "2020-04-01" @default.
• W3020227834 modified "2023-09-26" @default.
• W3020227834 title "A human joint-on-a-chip as alternative to animal models in osteoarthritis" @default.
• W3020227834 doi "https://doi.org/10.1016/j.joca.2020.02.135" @default.
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