2005
DOI: 10.1111/j.1600-6143.2005.00912.x
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Renal Ischemia/Reperfusion Injury Activates the Enhancer Domain of the Human Cytomegalovirus Major Immediate Early Promoter

Abstract: Reactivation of latent human cytomegalovirus is of significant concern in immunocompromised transplant

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Cited by 41 publications
(32 citation statements)
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“…These signals induce maturation of antigen-presenting cells in the graft that migrate to the lymph nodes and activate the adaptive arm of the immune response. NF-k B and AP-1 are activated by ischaemia/reperfusion injury and oxidative stress as well as inflammatory cytokines (Gloire et al, 2006;Kamata et al, 2005;Karin, 1995;Karin & Shaulian, 2001;Kim et al, 2005;Morgan & Liu, 2011;Oeckinghaus et al, 2011;Shaulian & Karin, 2002). In our studies, we observed very rapid activation of NF-k B and AP-1 family members, and biphasic activation of some pathways, including CD40, IL-6, NF-k B and JAK/STAT signalling Mechanisms of transplant-induced MCMV reactivation (Fig.…”
Section: Discussionsupporting
confidence: 50%
See 1 more Smart Citation
“…These signals induce maturation of antigen-presenting cells in the graft that migrate to the lymph nodes and activate the adaptive arm of the immune response. NF-k B and AP-1 are activated by ischaemia/reperfusion injury and oxidative stress as well as inflammatory cytokines (Gloire et al, 2006;Kamata et al, 2005;Karin, 1995;Karin & Shaulian, 2001;Kim et al, 2005;Morgan & Liu, 2011;Oeckinghaus et al, 2011;Shaulian & Karin, 2002). In our studies, we observed very rapid activation of NF-k B and AP-1 family members, and biphasic activation of some pathways, including CD40, IL-6, NF-k B and JAK/STAT signalling Mechanisms of transplant-induced MCMV reactivation (Fig.…”
Section: Discussionsupporting
confidence: 50%
“…While c-jun and c-fos are well-known oncoproteins with roles in cellular proliferation, junD is atypical of other AP-1 family members in both regulation of gene expression and in biological function (Hernandez et al, 2008). JunD is activated by oxidative stress, including renal ischaemia/reperfusion injury (Kim et al, 2005) and protects cells against apoptosis through upregulation of genes that mitigate oxidative damage (Gerald et al, 2004;Hernandez et al, 2008;Lamb et al, 2003;Pillebout et al, 2003;Tsuji, 2005). As with c-jun and c-fos, junD was rapidly activated by transplantation, but, in contrast to these proteins, junD activity was sustained for 48 h ( Fig.…”
Section: Discussionmentioning
confidence: 99%
“…Perhaps not surprisingly, inflammatory mediators such as tumor necrosis factor alpha (TNF-␣) and lipopolysaccharide (LPS), which are known to stimulate NF-B activation, are also stimulatory to the CMV MIE promoter in vitro (40,48,57). There are also numerous in vivo data, for animals as well as for human patients, which support this proposed mechanism (18,21,30,34,41,54). Although the preponderance of evidence supports the hypothesis that inflammation is linked to CMV reactivation, to date this causality has not been demonstrated in an in vivo system.…”
supporting
confidence: 51%
“…ROS production in response to RI/RI has been shown to stimulate the signal transduction pathway that activates expression of the transcription factor NF-κB, leading to the expression of numerous genes involving in inflammation (i.e., cytokines, chemokines, growth factors, immune receptors, cellular ligands, and adhesion molecules) [49]. Nuclear factor-kappa B plays a critical role in the pathophysiology of RI/RI, the accompanying inflammation and oxidative stress [49].…”
Section: Discussionmentioning
confidence: 99%