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: Carbon monoxide protects hepatocytes from TNF-alpha/Actinomycin D by inhibition of the caspase-8-mediated apoptotic pathway.
    Author: Kim HS, Loughran PA, Kim PK, Billiar TR, Zuckerbraun BS.
    Journal: Biochem Biophys Res Commun; 2006 Jun 16; 344(4):1172-8. PubMed ID: 16647044.
    Abstract:
    We have previously shown that carbon monoxide (CO) (250 ppm) prevented tumor necrosis factor-alpha (TNFalpha)-induced apoptosis and activated the transcription factor NF-kappaB in hepatocytes both in vivo and in vitro. These studies were conducted to further determine the mechanisms by which CO suppresses apoptotic signaling in TNFalpha (10 ng/ml) and Actinomycin D (ActD, 200 ng/ml)-treated hepatocytes. Consistent with our previous findings, CO protected against TNFalpha/ActD-induced cell death, which is in part dependent on NF-kappaB activation. This was associated with a reduction in mitochondrial damage, a decrease in cytochrome c release, and an inhibition of translocation of Bcl proteins to mitochondria. In conjugation with inhibition of these mitochondrial events, CO also suppressed caspases-8 and -3 cleavage in response to TNFalpha/ActD. Inhibition of NF-kappaB activation resulted in diminished CO-induced cFLIP expression and increased caspase-8 cleavage from cells treated with TNFalpha/ActD. These data indicate that CO interferes with apoptotic signaling at a proximal step.
    [Abstract] [Full Text] [Related] [New Search]