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Activation of extracellular signal-regulated kinase mediates apoptosis induced by uropathogenic Escherichia coli toxins via nitric oxide synthase: protective role of heme oxygenase-1

Chen, Ming ; Bao, Wenjie ; Aizman, Roman ; Huang, Ping ; Aspevall, Olle ; Gustafsson, Lars E ; Ceccatelli, Sandra ; Celsi, Gianni

The Journal of infectious diseases, 01 July 2004, Vol.190(1), pp.127-35 [Peer Reviewed Journal]

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  • Title:
    Activation of extracellular signal-regulated kinase mediates apoptosis induced by uropathogenic Escherichia coli toxins via nitric oxide synthase: protective role of heme oxygenase-1
  • Author: Chen, Ming ; Bao, Wenjie ; Aizman, Roman ; Huang, Ping ; Aspevall, Olle ; Gustafsson, Lars E ; Ceccatelli, Sandra ; Celsi, Gianni
  • Description: Pyelonephritis is a risk factor for renal tubular epithelial cell damage in children. The inter- and intracellular regulator nitric oxide (NO) plays a role in the modulation of cellular viability in urinary tract infections, but the role of the NO pathway in renal proximal tubular-cell death remains unclear. The present study demonstrates that, in renal epithelial cells undergoing death mediated by Escherichia coli strain ARD6 serotype O6K13H1 (O6), levels of the phosphorylated extracellular signal-regulated kinase (ERK) 1/2 and inducible NO synthase (iNOS) proteins are up-regulated, but levels of endothelial NO synthase are down-regulated. When NO synthase (NOS) activity is inhibited by the specific inhibitor of NOS or mitogen-activated protein kinase kinase, cells are prevented from death. Moreover, down-regulating protein 53 (p53) does not prevent the cells from dying, although p53 is up-regulated in O6-exposed cells. Up-regulation of heme oxygenase (HO)-1 by sodium nitroprusside or by the specific activator hemin inhibits cell death. In conclusion, the activation of ERK mediates O6 toxin-mediated renal cell death via induction of iNOS. Stimulation of HO-1 protects cells against death.
  • Is Part Of: The Journal of infectious diseases, 01 July 2004, Vol.190(1), pp.127-35
  • Identifier: ISSN: 0022-1899 ; PMID: 15195252 Version:1
  • Subjects: Apoptosis ; Bacterial Toxins -- Toxicity ; Escherichia Coli -- Pathogenicity ; Mitogen-Activated Protein Kinases -- Metabolism ; Nitric Oxide Synthase -- Metabolism
  • Language: English
  • Source: MEDLINE/PubMed (U.S. National Library of Medicine)

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