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• W2953207955 abstract "Background In osteoarthritis (OA), defects in cellular homeostasis, such as autophagy, are evident and precede joint damage (1). We have shown that there is a defect in autophagy in OA human chondrocytes and cartilage (2). Indeed, pharmacological activation of autophagy protects against joint damage (3). Our working hypothesis is that joint damage in OA could be due to a failure of autophagy that can be detected in the blood and tissue of patients. Objectives The objective of this study is to identify biomarkers associated with autophagy defects that could facilitate the development of personalized therapeutic strategies to prevent OA progression. Methods A comparative analysis of 35 autophagy genes was performed in blood from a Prospective OA Cohort of A Coruna (PROCOAC) of Non-OA and knee OA patients. Non-OA patients (Age: 61,44 ± 1,16 years; BMI: 25,25 ± 0,52; Females, n=18) and Knee OA patients (Age: 65,50 ± 1,05 years; BMI: 29,55 ± 0,67; Females, n=18, OA grade III-IV) were profiled using PrimePCR autophagy human panel array (Bio-Rad). Confirmatory studies of the candidate genes were performed in blood from Non-OA patients (Age: 60,13 ± 1,12 years; BMI: 24,85 ± 0,59; Females; n=30) and Knee-OA patients (Age: 68,4 ± 1,11 years; BMI: 29,65 ± 0,55; Females; n=30, OA grade III-IV) by Taqman Technology. A quantitative proteomic analysis of defective autophagy genes regulated upon deletion of Atg5 in human OA chondrocytes was performed by iTRAQ analysis. Moreover, the candidate gene was evaluated as a potential biomarker in human cartilage from Normal (n=19) and Knee-OA (n=20) patients and in both spontaneous aging (6, 12, 18, and 30 months old, n=3) and surgically-induced OA (10 weeks after surgery, n=4) in mice by immunohistochemistry. Remarkably, the consequences of candidate gene silencing on autophagy, FOXO signaling, inflammation, senescence and cell death by apoptosis was investigated by gene expression and flow cytometry. Results 15 autophagy-related genes were downregulated in blood from knee OA patients compared to non-OA patients (p 0.01), might be as a protective response, and increased NFκB and p16 expression (p Conclusion We identified biomarkers of defective autophagy as a mechanism of central homeostasis, which gives us a general vision of the disease mechanisms linked to OA clinical reality. References [1] Lotz MK, Carames B. Nat Rev Rheumatol. 2011;7:579-87 [2] Carames B, et al. Arthritis Rheum. 2010;62:791-801. [3] Carames B, et al. Ann Rheum Dis. 2012;71:575-81. Disclosure of Interests Irene Lorenzo: None declared, Jose Antonio Pinto Tasende: None declared, Natividad Oreiro: None declared, Francisco J. Blanco Consultant for: AbbVie, Bioiberica, BMS, GSK, Grunenthal, Janssen, Lilly, Pfizer, Regeneron, Roche, Sanofi, TRB Chemedica, and UCB, Beatriz Carames: None declared" @default.
• W2953207955 created "2019-06-27" @default.
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• W2953207955 date "2019-06-01" @default.
• W2953207955 modified "2023-09-26" @default.
• W2953207955 title "FRI0515 HSP90AA1, A CHAPERONE-MEDIATED AUTOPHAGY, IS A BIOMARKER ASSOCIATED WITH DEFECTIVE AUTOPHAGY IN OSTEOARTHRITIS" @default.
• W2953207955 doi "https://doi.org/10.1136/annrheumdis-2019-eular.4839" @default.
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