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: Activation of liver X receptors promotes inflammatory cytokine mRNA degradation by upregulation of tristetraprolin.
    Author: Xiao J, Chen Q, Tang D, Ou W, Wang J, Mo Z, Tang C, Peng L, Wang D.
    Journal: Acta Biochim Biophys Sin (Shanghai); 2017 Mar 01; 49(3):277-283. PubMed ID: 28119310.
    Abstract:
    Liver X receptors (LXRs) have anti-inflammatory properties. Whether LXRs play a role in post-transcriptional control of inflammatory cytokine expression is not clear. Here, we firstly identified that the synthetic LXR agonist T0901317 promoted IL-1β, IL-6 and TNFα mRNA degradation. Moreover, T0901317 destabilized TNFα mRNA through its 3'-untranslated region. In addition, T0901317 increased the expression of tristetraprolin (TTP), while antagonizing TTP with siRNA abrogated T0901317-mediated inflammatory cytokine mRNA decay. Interestingly, T0901317 repressed LPS-induced phosphorylation of ERK1/2 and p38 mitogen-activated protein kinase (MAPK) in THP-1 macrophages. The evidence presented here confirms that LXR activation with T0901317 inhibits the phosphorylation of ERK1/2 and p38 MAPK, likely resulting in the increased expression of TTP and the decay of LPS-induce inflammatory cytokine mRNAs.
    [Abstract] [Full Text] [Related] [New Search]