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• W2948118736 abstract "Osteoarthritis (OA) is a degenerative disease characterised by progressive loss ofarticular cartilage which affects millions of people globally. Although the leadingcauses of OA are still elusive, the increasing body of evidence indicates that thepredisposing factors such as lifestyle, age, injuries and genetics associated with theonset of OA. The regeneration of the degraded cartilage tissue in OA is mediated bythe tissue-resident stem cells. However, in advanced OA, the regenerative and tissuerepair capability of tissue-resident stem cells is compromised as a result of diseasescondition and leads to an unusual stem cell nature. Mesenchymal stem cells (MSCs)have been implicated in the pathogenesis of OA and, in turn, the progression of thedisease could be therapeutically modulated by MSCs. However, it remains unclearwhether the defective tissue-resident MSCs contributes to the pathogenesis of OA bya depleted stem cell pool or loss of the chondrogenic differentiation potential whichimpedes on the proper execution of stem cell functions. Therefore, this study aimed toexplore the biological properties of human non-OA and OA cartilage-derived MSCs(C-MSCs) as well as to determine whether the defects in human OA C-MSCs areresults of an inherent genetic make-up or acquired from the exposure of pathologicalOA inflammatory environment.A small fraction of non-weight bearing human articular cartilage from non-OAsubjects and OA patients were harvested during the arthroscopy session. Patients(n=11) were selected based on the grade 4 osteoarthritis according to the Kleegren andLawrence score system, and five cartilage samples were obtained from nonosteoarthriticdonors undergoing knee surgery or arthroscopy due to the sports injury.The optimised enzymatic digestion and serial plating methods were used to generate cartilage-derived MSCs. The differences in biological features of OA compared tonon-OA C-MSCs as well as that of non-OA C-MSCs cultured in OA synovial fluidwere investigated through a series of proliferation, cell cycle and apoptosis assays.The secretome profile and the global gene expression were performed throughcytokine antibody arrays and microarray, respectively.Mesenchymal stem cells were successfully generated from the human OA cartilagetissues along with non-OA cartilage. As compared to the human non-OA C-MSCs, thecounterpart from OA exhibited compromised cell qualities in term of ill-definedmorphology specifically at late passages, lower colony forming ability, reducedchondrogenesis when induced, a higher tendency towards osteogenic and adipogenicdifferentiation. However, the immunophenotypic profile between these two groupsremained relatively same. Additionally, human OA C-MSCs also demonstrated slowergrowth kinetics, prolonged doubling time, increased susceptibility to senescenceespecially at late passages, reduced proliferation and poor immunosuppressive abilityagainst T cells. It was also observed that during the in vitro culture expansion, thehuman OA C-MSCs underwent escalated level of cellular senescence in late passage(80%), apoptosis (i.e. 18.33±0.1% early apoptosis, 6.46±0.2% late apoptosis atpassage 3 and 20.09±0.1% early apoptosis, 8.42±0.2% late apoptosis at passage 6),exhibited G0/G1 cell cycle arrest (i.e. 78.68±3.17% of cells in G0/G1 phase, at passage3 while passage 6 had 93.23±2.64% of cells in G0/G1 phase) with a secretome profilethat reveals the downregulation of anti-inflammatory cytokines such as IL-1, IL-6, andIL-10, as well as aberrations in gene expression.Analysis of OA synovial fluid indicated with presence of proinflammatory cytokinesthat associated with OA pathophysiology while pre-treated non-OA C-MSCs with OAsynovial fluid exhibited increased apoptosis (i.e. 28.42±0.66% early apoptosis and12.11±0.47% late apoptosis) and inhibition of proliferation via cell cycle arrest(i.e.78.62±4.38% of cells in G0/G1 phase and 12.42±1.53% of cells in S phase). Thesefindings suggest that the catabolic and inflammatory agents in the synovial fluid couldbe implicated in cartilage tissue degradation, and may also be involved in the alterationof the inherent genetic makeup of cartilage tissue-resident MSCs which is evidentfrom the aberrant gene expression. The microarray-based gene expression analysis ofOA C-MSCs indicated dysregulation of essential genes of cell proliferation andsurvival, whereas the gene expression of non-OA MSCs treated with OA synovialfluid revealed dysregulation of cartilage metabolism. The KEGG pathway analysisbased on the dysregulated gene expression showed the involvement of several keysignalling pathways especially Wnt signalling, cell adhesion molecule pathway, Rassignalling pathway, cytokine-cytokine receptor interaction pathway.In conclusion, the biological features of OA C-MSCs are negatively affected by OAdisease. It could be possible that the inflammatory condition of OA synovial fluidimpedes the functional properties of cartilage tissue-resident MSCs. Thus, treatmentstrategies for OA should be strategized by allotting an appropriate concern to the inflammatory condition that limits the function of tissue stem cells and therapeuticallytransplanted stem cells." @default.
• W2948118736 created "2019-06-14" @default.
• W2948118736 creator A5017530001 @default.
• W2948118736 date "2018-02-01" @default.
• W2948118736 modified "2023-09-23" @default.
• W2948118736 title "Immunomodulatory and gene expression characterisation of human mesenchymal stem cells derived from non-osteoarthritic and osteoarthritic cartilage" @default.
• W2948118736 hasPublicationYear "2018" @default.
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