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• W2896540557 abstract "Abstract The retinal pigment epithelium ( RPE ) plays a central role in neuroretinal homoeostasis throughout life. Altered proteolysis and inflammatory processes involving RPE contribute to the pathophysiology of age‐related macular degeneration ( AMD ), but the link between these remains elusive. We report for the first time the effect of advanced glycation end products ( AGE )—known to accumulate on the ageing RPE 's underlying Bruch's membrane in situ—on both key lysosomal cathepsins and NF ‐ κB signalling in RPE . Cathepsin L activity and NF ‐ κB effector levels decreased significantly following 2‐week AGE exposure. Chemical cathepsin L inhibition also decreased total p65 protein levels, indicating that AGE ‐related change of NF ‐ κB effectors in RPE cells may be modulated by cathepsin L. However, upon TNF α stimulation, AGE ‐exposed cells had significantly higher ratio of phospho‐p65(Ser536)/total p65 compared to non‐ AGE d controls, with an even higher fold increase than in the presence of cathepsin L inhibition alone. Increased proportion of active p65 indicates an AGE ‐related activation of NF ‐ κB signalling in a higher proportion of cells and/or an enhanced response to TNF α. Thus, NF ‐ κB signalling modulation in the AGE d environment, partially regulated via cathepsin L, is employed by RPE cells as a protective (para‐inflammatory) mechanism but renders them more responsive to pro‐inflammatory stimuli." @default.
• W2896540557 created "2018-10-26" @default.
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• W2896540557 date "2018-10-19" @default.
• W2896540557 modified "2023-09-25" @default.
• W2896540557 title "Advanced glycation end products-related modulation of cathepsin L and NF-κB signalling effectors in retinal pigment epithelium lead to augmented response to TNFα" @default.
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• W2896540557 doi "https://doi.org/10.1111/jcmm.13944" @default.
• W2896540557 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6307775" @default.
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