FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2012785149> ?p ?o ?g. }

• W2012785149 endingPage "725" @default.
• W2012785149 startingPage "718" @default.
• W2012785149 abstract "The initiation and progression of several forms of retinal degenerations involve excessive, repetitive, and/or sustained oxidative stress that, in turn, mediate photoreceptor cell damage and death. Since phosphatidylinositol 3-kinase (PI3K)/Akt and mTOR/p70S6-kinase pathways are part of survival signaling in cells confronted with oxidative stress, we asked whether or not docosahexaenoic acid-derived neuroprotectin D1 (NPD1) mediates survival upon single-dose and/or repetitive oxidative stress through this pathway. For this purpose, we used human retinal pigment epithelial (ARPE-19) cells challenged by exposure to hydrogen peroxide (H(2)O(2)) plus tumor necrosis factor alpha (TNF-alpha). We found that in single-dose oxidative stress-induced apoptosis, phosphorylation of Akt, mTOR, and p70S6K was both time- and dose- dependent. Inhibition of PI3K or mTOR/p70S6K by wortmannin and rapamycin, respectively, increased apoptosis and inhibited phosphorylation of Akt and p70S6K induced by single-dose oxidative stress. While two exposures of a low dose, non-damaging oxidation induced apoptosis and upregulation of Akt, mTOR, and p70S6K, longer treatment of the cells with three exposures of low dose to low-dose stress showed no changes in the levels of Akt, mTOR, or p70S6K, and resulted in enhanced apoptosis compared to higher doses. Removing the oxidative stress-inducing agents following the single-dose or short term repetitive oxidative stress at the peak of Akt, mTOR, and p70S6K phosphorylation (i.e., 30 min after induction) led to recovery, with no apoptosis after 16 h of incubation. Cells that were induced with three low doses of stress did not show recovery when oxidative stress was removed 30 min after the last exposure. NPD1 protected the RPE cells against both single-dose and repetitive oxidative stress-induced apoptosis and promoted higher levels of phosphorylated Akt, mTOR, and p70S6K. Together, our results show that a) repetitive oxidative stress is dose dependent and may not be recovered by removing the oxidative stress-inducing agents, b) PI3K/Akt and mTOR/p70S6K pathways play a major role in the protection against oxidative stress-induced apoptosis in ARPE-19 cells, and c) NPD1 exerts protection under these conditions by inducing PI3K/Akt and mTOR/p70S6K pathways." @default.
• W2012785149 created "2016-06-24" @default.
• W2012785149 creator A5066891874 @default.
• W2012785149 creator A5068398524 @default.
• W2012785149 date "2010-06-01" @default.
• W2012785149 modified "2023-10-14" @default.
• W2012785149 title "PI3K/Akt and mTOR/p70S6K pathways mediate neuroprotectin D1-induced retinal pigment epithelial cell survival during oxidative stress-induced apoptosis" @default.
• W2012785149 cites W1739691545 @default.
• W2012785149 cites W1969871031 @default.
• W2012785149 cites W1974471174 @default.
• W2012785149 cites W1988668248 @default.
• W2012785149 cites W2002067726 @default.
• W2012785149 cites W2010306979 @default.
• W2012785149 cites W2013238661 @default.
• W2012785149 cites W2022004671 @default.
• W2012785149 cites W2028456697 @default.
• W2012785149 cites W2029150849 @default.
• W2012785149 cites W2033272889 @default.
• W2012785149 cites W2034922411 @default.
• W2012785149 cites W2036451354 @default.
• W2012785149 cites W2036663456 @default.
• W2012785149 cites W2045190167 @default.
• W2012785149 cites W2048661776 @default.
• W2012785149 cites W2057128909 @default.
• W2012785149 cites W2058488571 @default.
• W2012785149 cites W2070732456 @default.
• W2012785149 cites W2100726346 @default.
• W2012785149 cites W2103010344 @default.
• W2012785149 cites W2143187099 @default.
• W2012785149 cites W2148660876 @default.
• W2012785149 cites W2166550315 @default.
• W2012785149 cites W2186956122 @default.
• W2012785149 cites W2416826985 @default.
• W2012785149 cites W2738996050 @default.
• W2012785149 doi "https://doi.org/10.1016/j.exer.2010.03.002" @default.
• W2012785149 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2873108" @default.
• W2012785149 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20230819" @default.
• W2012785149 hasPublicationYear "2010" @default.
• W2012785149 type Work @default.
• W2012785149 sameAs 2012785149 @default.
• W2012785149 citedByCount "94" @default.
• W2012785149 countsByYear W20127851492012 @default.
• W2012785149 countsByYear W20127851492013 @default.
• W2012785149 countsByYear W20127851492014 @default.
• W2012785149 countsByYear W20127851492015 @default.
• W2012785149 countsByYear W20127851492016 @default.
• W2012785149 countsByYear W20127851492017 @default.
• W2012785149 countsByYear W20127851492018 @default.
• W2012785149 countsByYear W20127851492019 @default.
• W2012785149 countsByYear W20127851492020 @default.
• W2012785149 countsByYear W20127851492021 @default.
• W2012785149 countsByYear W20127851492022 @default.
• W2012785149 countsByYear W20127851492023 @default.
• W2012785149 crossrefType "journal-article" @default.
• W2012785149 hasAuthorship W2012785149A5066891874 @default.
• W2012785149 hasAuthorship W2012785149A5068398524 @default.
• W2012785149 hasBestOaLocation W20127851492 @default.
• W2012785149 hasConcept C11960822 @default.
• W2012785149 hasConcept C134018914 @default.
• W2012785149 hasConcept C185592680 @default.
• W2012785149 hasConcept C190283241 @default.
• W2012785149 hasConcept C2776151105 @default.
• W2012785149 hasConcept C2778308172 @default.
• W2012785149 hasConcept C31573885 @default.
• W2012785149 hasConcept C55493867 @default.
• W2012785149 hasConcept C75217442 @default.
• W2012785149 hasConcept C86554907 @default.
• W2012785149 hasConcept C86803240 @default.
• W2012785149 hasConcept C95444343 @default.
• W2012785149 hasConceptScore W2012785149C11960822 @default.
• W2012785149 hasConceptScore W2012785149C134018914 @default.
• W2012785149 hasConceptScore W2012785149C185592680 @default.
• W2012785149 hasConceptScore W2012785149C190283241 @default.
• W2012785149 hasConceptScore W2012785149C2776151105 @default.
• W2012785149 hasConceptScore W2012785149C2778308172 @default.
• W2012785149 hasConceptScore W2012785149C31573885 @default.
• W2012785149 hasConceptScore W2012785149C55493867 @default.
• W2012785149 hasConceptScore W2012785149C75217442 @default.
• W2012785149 hasConceptScore W2012785149C86554907 @default.
• W2012785149 hasConceptScore W2012785149C86803240 @default.
• W2012785149 hasConceptScore W2012785149C95444343 @default.
• W2012785149 hasIssue "6" @default.
• W2012785149 hasLocation W20127851491 @default.
• W2012785149 hasLocation W20127851492 @default.
• W2012785149 hasLocation W20127851493 @default.
• W2012785149 hasLocation W20127851494 @default.
• W2012785149 hasOpenAccess W2012785149 @default.
• W2012785149 hasPrimaryLocation W20127851491 @default.
• W2012785149 hasRelatedWork W2026238321 @default.
• W2012785149 hasRelatedWork W2050167066 @default.
• W2012785149 hasRelatedWork W2169526798 @default.
• W2012785149 hasRelatedWork W2334290869 @default.
• W2012785149 hasRelatedWork W2371839575 @default.
• W2012785149 hasRelatedWork W2392649720 @default.
• W2012785149 hasRelatedWork W2610344964 @default.
• W2012785149 hasRelatedWork W3030319632 @default.
• W2012785149 hasRelatedWork W4255550893 @default.
• W2012785149 hasRelatedWork W65266106 @default.

• next