FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2116623457> ?p ?o ?g. }

• W2116623457 abstract "Sterile inflammation occurs in the absence of live pathogens and is an unavoidable consequence of ischemia-reperfusion (IR) injury in the central nervous system (CNS). It is known that toll-like receptor 4 (Tlr4) contributes to damage and sterile inflammation in the CNS mediated by IR. However, the mechanism of Tlr4 activation under sterile conditions in ischemic tissue is poorly understood. We performed this study to clarify the mechanism. To this end, we focused on the extracellular heat shock protein 70 (Hsp70), the prototypic Tlr4 ligand.Tlr4-, Myd88- and Trif-knockout animals, as well as C57BL/6 mice, were used for the wild type control. For the in vivo study, we used a mouse model of retinal IR injury. To test the role of protein kinase C (PKC) in IR injury, IR retinas were treated with the PKC inhibitors (polymyxin B and Gö6976) and retinal damage was evaluated by directly counting neurons in the ganglion cell layer of flat-mounted retinas seven days after IR. Primary retinal neurons (retinal ganglion cells) and glial cells were used for in vitro experiments. Quantitative RT-PCR, ELISA and western blot analysis were used to study the production of pro-inflammatory factors in IR retinas and in primary cell cultures.We found significant accumulation of extracellular Hsp70 in a model of retinal IR injury. We noted that PKC was involved in Tlr4 signaling, and found that PKC inhibitors promoted neuroprotection by reducing pro-inflammatory activity in ischemic tissue. To put all of the pieces in the signaling cascade together, we performed an in vitro study. We found that PKC was critical to mediate the Hsp70-dependent pro-inflammatory response. At the same time, the contamination of Hsp70 preparations with low-dose endotoxin was not critical to mediate the production of pro-inflammatory factors. We found that extracellular Hsp70 can promote neuronal death at least, by mediating production of cytotoxic levels of tumor necrosis factor alpha, predominantly due to the Tlr4/Myd88 signaling cascade.Our findings suggest that PKC acts as a switch to amplify the pro-inflammatory activity of Hsp70/Tlr4 signaling, which is sufficient to mediate neuronal death." @default.
• W2116623457 created "2016-06-24" @default.
• W2116623457 creator A5008007699 @default.
• W2116623457 creator A5037523967 @default.
• W2116623457 creator A5043655945 @default.
• W2116623457 creator A5066765586 @default.
• W2116623457 creator A5069269239 @default.
• W2116623457 date "2014-04-23" @default.
• W2116623457 modified "2023-10-05" @default.
• W2116623457 title "Putative role of protein kinase C in neurotoxic inflammation mediated by extracellular heat shock protein 70 after ischemia-reperfusion" @default.
• W2116623457 cites W106111299 @default.
• W2116623457 cites W143574421 @default.
• W2116623457 cites W1515599953 @default.
• W2116623457 cites W1547043719 @default.
• W2116623457 cites W1577885098 @default.
• W2116623457 cites W1973265746 @default.
• W2116623457 cites W1973404097 @default.
• W2116623457 cites W1978862885 @default.
• W2116623457 cites W1981010107 @default.
• W2116623457 cites W1982422365 @default.
• W2116623457 cites W1983419107 @default.
• W2116623457 cites W1990249993 @default.
• W2116623457 cites W1997612327 @default.
• W2116623457 cites W1997899019 @default.
• W2116623457 cites W1999064607 @default.
• W2116623457 cites W2005570998 @default.
• W2116623457 cites W2009091430 @default.
• W2116623457 cites W2019979594 @default.
• W2116623457 cites W2027731275 @default.
• W2116623457 cites W2027825684 @default.
• W2116623457 cites W2034406849 @default.
• W2116623457 cites W2035336513 @default.
• W2116623457 cites W2042851093 @default.
• W2116623457 cites W2045098547 @default.
• W2116623457 cites W2048922948 @default.
• W2116623457 cites W2059464380 @default.
• W2116623457 cites W2064243077 @default.
• W2116623457 cites W2064836052 @default.
• W2116623457 cites W2081885526 @default.
• W2116623457 cites W2083747483 @default.
• W2116623457 cites W2086776938 @default.
• W2116623457 cites W2109491705 @default.
• W2116623457 cites W2111323052 @default.
• W2116623457 cites W2115757439 @default.
• W2116623457 cites W2118200665 @default.
• W2116623457 cites W2121684383 @default.
• W2116623457 cites W2133449490 @default.
• W2116623457 cites W2142345534 @default.
• W2116623457 cites W2147259348 @default.
• W2116623457 cites W2150594596 @default.
• W2116623457 cites W2150679087 @default.
• W2116623457 cites W2151970419 @default.
• W2116623457 cites W2153517367 @default.
• W2116623457 cites W2157339124 @default.
• W2116623457 cites W2371948111 @default.
• W2116623457 doi "https://doi.org/10.1186/1742-2094-11-81" @default.
• W2116623457 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4001362" @default.
• W2116623457 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24755298" @default.
• W2116623457 hasPublicationYear "2014" @default.
• W2116623457 type Work @default.
• W2116623457 sameAs 2116623457 @default.
• W2116623457 citedByCount "33" @default.
• W2116623457 countsByYear W21166234572014 @default.
• W2116623457 countsByYear W21166234572015 @default.
• W2116623457 countsByYear W21166234572016 @default.
• W2116623457 countsByYear W21166234572017 @default.
• W2116623457 countsByYear W21166234572018 @default.
• W2116623457 countsByYear W21166234572019 @default.
• W2116623457 countsByYear W21166234572020 @default.
• W2116623457 countsByYear W21166234572022 @default.
• W2116623457 countsByYear W21166234572023 @default.
• W2116623457 crossrefType "journal-article" @default.
• W2116623457 hasAuthorship W2116623457A5008007699 @default.
• W2116623457 hasAuthorship W2116623457A5037523967 @default.
• W2116623457 hasAuthorship W2116623457A5043655945 @default.
• W2116623457 hasAuthorship W2116623457A5066765586 @default.
• W2116623457 hasAuthorship W2116623457A5069269239 @default.
• W2116623457 hasBestOaLocation W21166234571 @default.
• W2116623457 hasConcept C104317684 @default.
• W2116623457 hasConcept C169760540 @default.
• W2116623457 hasConcept C195794163 @default.
• W2116623457 hasConcept C203014093 @default.
• W2116623457 hasConcept C205260736 @default.
• W2116623457 hasConcept C2776070231 @default.
• W2116623457 hasConcept C2776914184 @default.
• W2116623457 hasConcept C2777093970 @default.
• W2116623457 hasConcept C2777624874 @default.
• W2116623457 hasConcept C28406088 @default.
• W2116623457 hasConcept C55493867 @default.
• W2116623457 hasConcept C62478195 @default.
• W2116623457 hasConcept C86803240 @default.
• W2116623457 hasConcept C95444343 @default.
• W2116623457 hasConceptScore W2116623457C104317684 @default.
• W2116623457 hasConceptScore W2116623457C169760540 @default.
• W2116623457 hasConceptScore W2116623457C195794163 @default.
• W2116623457 hasConceptScore W2116623457C203014093 @default.
• W2116623457 hasConceptScore W2116623457C205260736 @default.
• W2116623457 hasConceptScore W2116623457C2776070231 @default.
• W2116623457 hasConceptScore W2116623457C2776914184 @default.
• W2116623457 hasConceptScore W2116623457C2777093970 @default.

• next