FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2940661663> ?p ?o ?g. }

• W2940661663 abstract "Inflammation and oxidative stress are common factors involved in the pathogenesis of retinal diseases, such as aged-related macular degeneration and diabetic retinopathy. Autophagy is a catabolic process essential to cell survival in response to stress. This process is highly active in retinal pigment epithelium (RPE) cells. Our previous findings demonstrated that lipopolysaccharide (LPS) induces an inflammatory response of RPE cells that implies classical phospholipases D (PLD1 and 2) activation, cyclooxygenase-2 (COX-2) expression, prostaglandin E2 production and reduced cell viability. In this work we studied the autophagic process and its modulation by the PLD pathway in D407 and ARPE-19 RPE cells exposed to the LPS-induced inflammatory model. LPS (10 μg/ml or 25 μg/ml) exposure for 24 h increased LC3-II content (an autophagy marker) and LC3-positive punctate structures in both RPE cell lines studied. Next, the drug Bafilomycin A1 (BAF, 50 nM) was used to block the autophagic flux. In cells pre-incubated with BAF, LC3-II and sequestosome 1 (SQSTM1/p62) levels and autophagosome-like structures were increased by LPS, demonstrating that the inflammatory injury increases the autophagic process in RPE cells. To study the role of the PLD pathway, cells were pre-incubated for 1 h with selective PLD1 (VU0359595) or PLD2 (VU0285655-1) inhibitors prior to LPS addition. Under control condition LC3-positive punctate structures were increased in cells pre-incubated with PLD2 inhibitor while with PLD1 inhibitor they increased in cells exposed to LPS. MTT reduction assays showed that early autophagy inhibitors, 3-methyladenin (3-MA) and LY294002, enhanced the loss in cell viability induced by LPS exposure for 48 h. On the contrary, the inhibition of PLD1 and PLD2 prevented the loss in cell viability induced by LPS. In conclusion, our results show that even though LPS treatment promotes an inflammatory response in RPE cells, it also triggers the activation of the autophagic process which in turn may serve as a protective mechanism for the cells. In addition, we demonstrate that the PLD pathway modulates the autophagic process in RPE cells. Our findings contribute to the knowledge of the molecular basis of retinal inflammatory and degenerative diseases and open new avenues for potential therapeutic exploration." @default.
• W2940661663 created "2019-05-03" @default.
• W2940661663 creator A5007656211 @default.
• W2940661663 creator A5011935790 @default.
• W2940661663 creator A5020923264 @default.
• W2940661663 creator A5079667888 @default.
• W2940661663 date "2019-04-24" @default.
• W2940661663 modified "2023-10-16" @default.
• W2940661663 title "Lipopolysaccharide-Induced Autophagy Mediates Retinal Pigment Epithelium Cells Survival. Modulation by the Phospholipase D Pathway" @default.
• W2940661663 cites W1438640379 @default.
• W2940661663 cites W1523693806 @default.
• W2940661663 cites W1593266928 @default.
• W2940661663 cites W1608040782 @default.
• W2940661663 cites W1816585441 @default.
• W2940661663 cites W1884934928 @default.
• W2940661663 cites W1965203292 @default.
• W2940661663 cites W1968444524 @default.
• W2940661663 cites W1972686405 @default.
• W2940661663 cites W1978479234 @default.
• W2940661663 cites W1984186519 @default.
• W2940661663 cites W1985029869 @default.
• W2940661663 cites W1987951940 @default.
• W2940661663 cites W1992643412 @default.
• W2940661663 cites W1993159760 @default.
• W2940661663 cites W1993873224 @default.
• W2940661663 cites W1995610541 @default.
• W2940661663 cites W2004424917 @default.
• W2940661663 cites W2006896973 @default.
• W2940661663 cites W2018289835 @default.
• W2940661663 cites W2018719587 @default.
• W2940661663 cites W2020401974 @default.
• W2940661663 cites W2025364264 @default.
• W2940661663 cites W2031084334 @default.
• W2940661663 cites W2034623405 @default.
• W2940661663 cites W2037386621 @default.
• W2940661663 cites W2045516425 @default.
• W2940661663 cites W2049784637 @default.
• W2940661663 cites W2051241024 @default.
• W2940661663 cites W2052101846 @default.
• W2940661663 cites W2056029075 @default.
• W2940661663 cites W2065233558 @default.
• W2940661663 cites W2068602754 @default.
• W2940661663 cites W2074969762 @default.
• W2940661663 cites W2089871870 @default.
• W2940661663 cites W2100837269 @default.
• W2940661663 cites W2111135552 @default.
• W2940661663 cites W2111274886 @default.
• W2940661663 cites W2122366541 @default.
• W2940661663 cites W2128635872 @default.
• W2940661663 cites W2134555179 @default.
• W2940661663 cites W2135086572 @default.
• W2940661663 cites W2142432153 @default.
• W2940661663 cites W2154363497 @default.
• W2940661663 cites W2158450596 @default.
• W2940661663 cites W2163643821 @default.
• W2940661663 cites W2164362108 @default.
• W2940661663 cites W2165439370 @default.
• W2940661663 cites W2230332290 @default.
• W2940661663 cites W2238034293 @default.
• W2940661663 cites W2264982258 @default.
• W2940661663 cites W2267713729 @default.
• W2940661663 cites W2275879522 @default.
• W2940661663 cites W2303528609 @default.
• W2940661663 cites W2331076767 @default.
• W2940661663 cites W2337213331 @default.
• W2940661663 cites W2431321293 @default.
• W2940661663 cites W2532748192 @default.
• W2940661663 cites W2566416357 @default.
• W2940661663 cites W2569274667 @default.
• W2940661663 cites W2569601267 @default.
• W2940661663 cites W2581549657 @default.
• W2940661663 cites W2593816418 @default.
• W2940661663 cites W2602573314 @default.
• W2940661663 cites W2661082659 @default.
• W2940661663 cites W2735527928 @default.
• W2940661663 cites W2751189719 @default.
• W2940661663 cites W2752326209 @default.
• W2940661663 cites W2782440864 @default.
• W2940661663 cites W2794819229 @default.
• W2940661663 cites W2883221415 @default.
• W2940661663 cites W2891111520 @default.
• W2940661663 cites W4293247451 @default.
• W2940661663 doi "https://doi.org/10.3389/fncel.2019.00154" @default.
• W2940661663 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6497095" @default.
• W2940661663 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31327962" @default.
• W2940661663 hasPublicationYear "2019" @default.
• W2940661663 type Work @default.
• W2940661663 sameAs 2940661663 @default.
• W2940661663 citedByCount "15" @default.
• W2940661663 countsByYear W29406616632019 @default.
• W2940661663 countsByYear W29406616632020 @default.
• W2940661663 countsByYear W29406616632021 @default.
• W2940661663 countsByYear W29406616632022 @default.
• W2940661663 countsByYear W29406616632023 @default.
• W2940661663 crossrefType "journal-article" @default.
• W2940661663 hasAuthorship W2940661663A5007656211 @default.
• W2940661663 hasAuthorship W2940661663A5011935790 @default.
• W2940661663 hasAuthorship W2940661663A5020923264 @default.
• W2940661663 hasAuthorship W2940661663A5079667888 @default.
• W2940661663 hasBestOaLocation W29406616631 @default.

• next