[Signal transduction abnormalities in systemic lupus erythematosus].

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  • Author(s): Nagy G;Nagy G; Géher P; Koncz A; Perl A
  • Source:
    Orvosi hetilap [Orv Hetil] 2005 Jul 31; Vol. 146 (31), pp. 1625-30.
  • Publication Type:
    English Abstract; Journal Article; Review
  • Language:
    Hungarian
  • Additional Information
    • Transliterated Title:
      Jelátviteli defektusok szisztémás lupus erythematosusban.
    • Source:
      Publisher: Akademiai Kiado Country of Publication: Hungary NLM ID: 0376412 Publication Model: Print Cited Medium: Print ISSN: 0030-6002 (Print) Linking ISSN: 00306002 NLM ISO Abbreviation: Orv Hetil Subsets: MEDLINE
    • Publication Information:
      Publication: 2007- : Budapest : Akademiai Kiado
      Original Publication: Pest : Markusovszky Lajos
    • Subject Terms:
      Signal Transduction*; Calcium/*metabolism ; Lupus Erythematosus, Systemic/*metabolism ; Mitochondria/*metabolism ; Nitric Oxide/*metabolism ; T-Lymphocytes/*metabolism; Calcium Channels/metabolism ; Humans ; Lymphocyte Activation
    • Abstract:
      Engagement of T cell receptors by antigen-presenting cells or stimulation by cytokines determine whether the cell will become activated, anergic or die via apoptosis or necrosis. Ca2+ is a key second messenger that delivers signal from the cell surface, reactive oxygen intermediates and nitric oxide are recently recognized as important mediators of T cell activation. Nitric oxide is a multifunctional intracellular and intercellular messenger induces mitochondrial biogenesis in many cell types, such as lymphocytes. Mitochondria produce reactive oxygen intermediates and store and release Ca2+ in response to activation and death signals. Rapid Ca2+ fluxing is increased while sustained Ca2+ signaling is decreased in lupus T cells. Lupus T cells contain increased numbers and mass of mitochondria. Serum nitric oxide levels and production of nitric oxide by monocytes is increased in patients with systemic lupus erythematosus. Lupus T cells exhibit mitochondrial hyperpolarization and increased mitochondrial mass, which confer predisposition to necrosis rather than apoptosis in response to repetitive activation and death signals. Exposure of normal T cells to nitric oxide dose-dependently increase the mitochondrial mass and mimic rapid and sustained Ca2+ signal abnormalities observed in lupus T cells. Thus increased mitochondrial biogenesis may account for altered Ca2+ handling and represents novel targets for pharmacological intervention in SLE.
    • Number of References:
      49
    • Accession Number:
      0 (Calcium Channels)
      31C4KY9ESH (Nitric Oxide)
      SY7Q814VUP (Calcium)
    • Publication Date:
      Date Created: 20050915 Date Completed: 20051101 Latest Revision: 20131121
    • Publication Date:
      20240829
    • Accession Number:
      16158611