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10.3390/toxins10030124 http://scihub22266oqcxt.onion/10.3390/toxins10030124 C5869412!5869412 !29543732     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29543732 &cmd=llinks): Failed to open stream: HTTP request failed! 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Indoxyl Sulfate Promotes Macrophage IL-1? Production by Activating Aryl Hydrocarbon Receptor/NF-?/MAPK Cascades, but the NLRP3 inflammasome Was Not Activated |pdf=|usr=}}{{29543732 }} gab.com Text Indoxyl Sulfate Promotes Macrophage IL-1 Production by Activating Aryl Hydrocarbon Receptor/NF- /MAPK Cascades, but the NLRP3 inflammasome Was Not Activated JO: Toxins (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=29543732 #FOAvip In chronic kidney disease (CKD) patients, accumulation of uremic toxins is associated with cardiovascular risk and mortality. One of the hallmarks of kidney disease-related cardiovascular disease is intravascular macrophage inflammation, but the mechanism of the reaction with these toxins is not completely understood. Macrophages differentiated from THP-1 cells were exposed to indoxyl sulfate (IS), a representative uremic toxin, and changes in inflammatory cytokine production and intracellular signaling molecules including interleukin (IL)-1, aryl hydrocarbon receptor (AhR), nuclear factor (NF)-?, and mitogen-activated protein kinase (MAPK) cascades as well as the NLRP3 inflammasome were quantified by real-time PCR, Western blot analysis, and enzyme-linked immunosorbent assay. IS induced macrophage pro-IL-1? mRNA expression, although mature IL-1 was only slightly increased. IS increased AhR and the AhR-related mRNA expression; this change was suppressed by administration of proteasome inhibitor. IS promoted phosphorylation of NF-?B p65 and MAPK enzymes; the reaction and IL-1 expression were inhibited by BAY11-7082, an inhibitor of NF-?B. In contrast, IS decreased NLRP3 and did not change ASC, pro-caspase 1, or caspase-1 activation. IS-inducing inflammation in macrophages results from accelerating AhR-NF-?B/MAPK cascades, but the NLRP3 inflammasome was not activated. These reactions may restrict mature IL-1? production, which may explain sustained chronic inflammation in CKD patients. Twit Text FOAVip Indoxyl Sulfate Promotes Macrophage IL-1 Production by Activating Aryl Hydrocarbon Receptor/NF- /MAPK Cascades, but the NLRP3 inflammasome Was Not Activated ????Toxins (Basel) http://www.kidney.de/pget.php?&tw=1&pmid=29543732 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29543732 #FOAvip English Wikipedia <ref>{{Cite pmid|29543732 }}</ref> Indoxyl Sulfate Promotes Macrophage IL-1? Production by Activating Aryl Hydrocarbon Receptor/NF-?/MAPK Cascades, but the NLRP3 inflammasome Was Not Activated #MMPMID29543732 Wakamatsu T ; Yamamoto S ; Ito T ; Sato Y ; Matsuo K ; Takahashi Y ; Kaneko Y ; Goto S ; Kazama JJ ; Gejyo F ; Narita I Toxins (Basel) 2018[Mar]; 10 (3 ): ä PMID29543732 show ga In chronic kidney disease (CKD) patients, accumulation of uremic toxins is associated with cardiovascular risk and mortality. One of the hallmarks of kidney disease-related cardiovascular disease is intravascular macrophage inflammation, but the mechanism of the reaction with these toxins is not completely understood. Macrophages differentiated from THP-1 cells were exposed to indoxyl sulfate (IS), a representative uremic toxin, and changes in inflammatory cytokine production and intracellular signaling molecules including interleukin (IL)-1, aryl hydrocarbon receptor (AhR), nuclear factor (NF)-?, and mitogen-activated protein kinase (MAPK) cascades as well as the NLRP3 inflammasome were quantified by real-time PCR, Western blot analysis, and enzyme-linked immunosorbent assay. IS induced macrophage pro-IL-1? mRNA expression, although mature IL-1 was only slightly increased. IS increased AhR and the AhR-related mRNA expression; this change was suppressed by administration of proteasome inhibitor. IS promoted phosphorylation of NF-?B p65 and MAPK enzymes; the reaction and IL-1 expression were inhibited by BAY11-7082, an inhibitor of NF-?B. In contrast, IS decreased NLRP3 and did not change ASC, pro-caspase 1, or caspase-1 activation. IS-inducing inflammation in macrophages results from accelerating AhR-NF-?B/MAPK cascades, but the NLRP3 inflammasome was not activated. These reactions may restrict mature IL-1? production, which may explain sustained chronic inflammation in CKD patients. |Humans [MESH] |Indican/*pharmacology [MESH] |Interleukin-1beta/genetics/*metabolism [MESH] |Macrophages/*drug effects/metabolism [MESH] |Mitogen-Activated Protein Kinases/*metabolism [MESH] |NF-kappa B/*metabolism [MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/metabolism [MESH] |Receptors, Aryl Hydrocarbon/genetics/*metabolism [MESH] |Signal Transduction [MESH]Indoxyl Sulfate Promotes Macrophage IL-1? Production by Activating Ary(epmc).pdf DeepDyve Pubget Overpricing