These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Effect of tumor necrosis factor-alpha and interleukin-1 alpha on heme oxygenase-1 expression in human endothelial cells.
    Author: Terry CM, Clikeman JA, Hoidal JR, Callahan KS.
    Journal: Am J Physiol; 1998 Mar; 274(3):H883-91. PubMed ID: 9530200.
    Abstract:
    Heme iron exacerbates oxidant damage by catalyzing the production of free radicals. Heme oxygenase is the rate-limiting enzyme involved in heme catabolism. An inducible form of heme oxygenase, heme oxygenase-1 (HO-1), is upregulated in oxidant and inflammatory settings, and recent work suggests that HO-1 induction may serve a protective function against oxidant injury. The ability of the endogenous inflammatory mediators, interleukin (IL)-1 alpha, tumor necrosis factor-alpha (TNF-alpha), and IL-6, to enhance HO-1 expression in cultured human endothelial cells was examined in this study. HO-1 mRNA and protein expression were upregulated by IL-1 alpha and TNF-alpha exposure but not by IL-6. Induction of HO-1 mRNA by IL-1 alpha and TNF-alpha occurred in a concentration- and time-dependent fashion, with maximal expression occurring by 4 h for both cytokines. Induction depended on protein synthesis and occurred at the transcriptional level. Inhibition of the AP-1 transcription factor with curcumin decreased the cytokine induction of HO-1 mRNA, suggesting the involvement of this transcription factor in cytokine signaling of HO-1. The results of this study indicate that the endogenous inflammatory cytokines IL-1 alpha and TNF-alpha induce HO-1 in endothelial cells, providing further evidence that HO-1 may be an important cellular response to inflammatory stress.
    [Abstract] [Full Text] [Related] [New Search]