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10.1111/ajt.12711 http://scihub22266oqcxt.onion/10.1111/ajt.12711 C4074706!4074706!24903305     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24903305&cmd=llinks): Failed to open stream: HTTP request failed! 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ATF6 Mediates a Pro-inflammatory Synergy between ER Stress and TLR Activation in the Pathogenesis of Liver Ischemia Reperfusion Injury |pdf=|usr=}}{{24903305}} gab.com Text ATF6 Mediates a Pro-inflammatory Synergy between ER Stress and TLR Activation in the Pathogenesis of Liver Ischemia Reperfusion Injury JO: Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=24903305 #FOAvip Although roles of the metabolic stress in organ ischemia reperfusion injury (IRI) have been well recognized, the question of whether and how these stress responses regulate innate immune activation against IR remains unclear. In a murine liver partial warm ischemia mode, we showed that prolonged ischemia triggered endoplasmic reticulum (ER) stress response, particularly, the ATF6 branch, in liver Kupffer cells and altered their responsiveness against TLR stimulation. Ischemia-primed cells increased pro-, but decreased anti-, inflammatory cytokine productions. Alleviation of ER stress in vivo by small chemical chaperon 4-phenylbutyrate or ATF6 siRNA diminished the pro-inflammatory priming effect of ischemia in KCs, leading to the inhibition of liver immune response against IR and protection of livers from IRI. In vitro, ATF6 siRNA abrogated the ER stress-mediated pro-inflammatory enhancement of macrophage TLR4 response, by restricting NF-kB and restoring Akt activations. Thus, ischemia primes liver innate immune cells by ATF6-mediated ER stress response. The IR-induced metabolic stress and TLR activation function in synergy to activate tissue inflammatory immune response. Twit Text FOAVip ATF6 Mediates a Pro-inflammatory Synergy between ER Stress and TLR Activation in the Pathogenesis of Liver Ischemia Reperfusion Injury ????Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=24903305 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24903305 #FOAvip English Wikipedia <ref>{{Cite pmid|24903305}}</ref> ATF6 Mediates a Pro-inflammatory Synergy between ER Stress and TLR Activation in the Pathogenesis of Liver Ischemia Reperfusion Injury #MMPMID24903305 Rao J; Yue S; Fu Y; Zhu J; Wang X; Busuttil RW; Kupiec-Weglinski JW; Lu L; Zhai Y Am J Transplant 2014[Jul]; 14 (7): 1552-61 PMID24903305show ga Although roles of the metabolic stress in organ ischemia reperfusion injury (IRI) have been well recognized, the question of whether and how these stress responses regulate innate immune activation against IR remains unclear. In a murine liver partial warm ischemia mode, we showed that prolonged ischemia triggered endoplasmic reticulum (ER) stress response, particularly, the ATF6 branch, in liver Kupffer cells and altered their responsiveness against TLR stimulation. Ischemia-primed cells increased pro-, but decreased anti-, inflammatory cytokine productions. Alleviation of ER stress in vivo by small chemical chaperon 4-phenylbutyrate or ATF6 siRNA diminished the pro-inflammatory priming effect of ischemia in KCs, leading to the inhibition of liver immune response against IR and protection of livers from IRI. In vitro, ATF6 siRNA abrogated the ER stress-mediated pro-inflammatory enhancement of macrophage TLR4 response, by restricting NF-kB and restoring Akt activations. Thus, ischemia primes liver innate immune cells by ATF6-mediated ER stress response. The IR-induced metabolic stress and TLR activation function in synergy to activate tissue inflammatory immune response. äATF6 Mediates a Pro-inflammatory Synergy between ER Stress and TLR Act(epmc).pdf DeepDyve Pubget Overpricing