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10.1155/2020/6357046 http://scihub22266oqcxt.onion/10.1155/2020/6357046 32089648!7013356!32089648     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32089648&cmd=llinks): Failed to open stream: HTTP request failed! 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CD154 Induces Interleukin-6 Secretion by Kidney Tubular Epithelial Cells under Hypoxic Conditions: Inhibition by Chloroquine |pdf=|usr=}}{{32089648}} gab.com Text CD154 Induces Interleukin-6 Secretion by Kidney Tubular Epithelial Cells under Hypoxic Conditions: Inhibition by Chloroquine JO: Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=32089648 #FOAvip Inflammation is a major contributor to tubular epithelium injury in kidney disorders, and the involvement of blood platelets in driving inflammation is increasingly stressed. CD154, the ligand of CD40, is one of the mediators supporting platelet proinflammatory properties. Although hypoxia is an essential constituent of the inflammatory reaction, if and how platelets and CD154 regulate inflammation in hypoxic conditions remain unclear. Here, we studied the control by CD154 of the proinflammatory cytokine interleukin- (IL-) 6 secretion in short-term oxygen (O(2)) deprivation conditions, using the HK-2 cell line as a kidney tubular epithelial cell (TEC) model. IL-6 secretion was markedly stimulated by CD154 after 1 to 3 hours of hypoxic stress. Both intracellular IL-6 expression and secretion were stimulated by CD154 and associated with a strong upregulation of IL-6 mRNA and increased transcription. Searching for inhibitors of CD154-mediated IL-6 production by HK-2 cells in hypoxic conditions, we observed that chloroquine, a drug that has been repurposed as an anti-inflammatory agent, alleviated this induction. Therefore, CD154 is a potent early stimulus for IL-6 secretion by TECs in O(2) deprivation conditions, a mechanism likely to take part in the deleterious inflammatory consequences of platelet activation in kidney tubular injury. The inhibition of CD154-induced IL-6 production by chloroquine suggests the potential usefulness of this drug as a therapeutic adjunct in conditions associated with acute kidney injury. Twit Text FOAVip CD154 Induces Interleukin-6 Secretion by Kidney Tubular Epithelial Cells under Hypoxic Conditions: Inhibition by Chloroquine ????Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=32089648 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32089648 #FOAvip English Wikipedia <ref>{{Cite pmid|32089648}}</ref> CD154 Induces Interleukin-6 Secretion by Kidney Tubular Epithelial Cells under Hypoxic Conditions: Inhibition by Chloroquine #MMPMID32089648 Dewitte A; Villeneuve J; Lepreux S; Bouchecareilh M; Gauthereau X; Rigothier C; Combe C; Ouattara A; Ripoche J Mediators Inflamm 2020[]; 2020 (ä): 6357046 PMID32089648show ga Inflammation is a major contributor to tubular epithelium injury in kidney disorders, and the involvement of blood platelets in driving inflammation is increasingly stressed. CD154, the ligand of CD40, is one of the mediators supporting platelet proinflammatory properties. Although hypoxia is an essential constituent of the inflammatory reaction, if and how platelets and CD154 regulate inflammation in hypoxic conditions remain unclear. Here, we studied the control by CD154 of the proinflammatory cytokine interleukin- (IL-) 6 secretion in short-term oxygen (O(2)) deprivation conditions, using the HK-2 cell line as a kidney tubular epithelial cell (TEC) model. IL-6 secretion was markedly stimulated by CD154 after 1 to 3 hours of hypoxic stress. Both intracellular IL-6 expression and secretion were stimulated by CD154 and associated with a strong upregulation of IL-6 mRNA and increased transcription. Searching for inhibitors of CD154-mediated IL-6 production by HK-2 cells in hypoxic conditions, we observed that chloroquine, a drug that has been repurposed as an anti-inflammatory agent, alleviated this induction. Therefore, CD154 is a potent early stimulus for IL-6 secretion by TECs in O(2) deprivation conditions, a mechanism likely to take part in the deleterious inflammatory consequences of platelet activation in kidney tubular injury. The inhibition of CD154-induced IL-6 production by chloroquine suggests the potential usefulness of this drug as a therapeutic adjunct in conditions associated with acute kidney injury. |Apoptosis[MESH] |Blotting, Western[MESH] |CD40 Ligand/*pharmacology[MESH] |Cell Hypoxia/*physiology[MESH] |Cell Line[MESH] |Cell Proliferation[MESH] |Cell Survival[MESH] |Chloroquine/*pharmacology[MESH] |Enzyme-Linked Immunosorbent Assay[MESH] |Epithelial Cells/*drug effects/*metabolism[MESH] |Flow Cytometry[MESH] |Humans[MESH] |Interleukin-6/*metabolism[MESH] |Kidney Tubules/*cytology[MESH] |Microscopy, Fluorescence[MESH]CD154 Induces Interleukin-6 Secretion by Kidney Tubular Epithelial Cel(epmc).pdf DeepDyve Pubget Overpricing