Polyamine-mediated post-transcriptional regulation of COX-2

The effects of environmental factors on the virulence of Trichomonas vaginalis

“…In T. vaginalis, the TveIF-5A factor may be part of a posttranscriptional regulatory mechanism mediated by polyamines similar to the one reported for human cyclooxygenase-2 gene (cox-2), where a mature hypusinated-eIF-5A protein interacts with a stem-loop RNA structure, an eIF-5A Response Element (ERE), located at the 3 0 -UTR of the cox-2 mRNA, affecting its stability, downstream RNA processing, and translation into protein [78]. A similar mechanism of post-transcriptional regulation mediated by RNAeprotein interactions has been proposed for the polyamine-mediated expression of the cytotoxic TvCP39, because an ERE-like stem-loop structure was found in the 3 0 -UTR region of its mRNA [46] (unpublished); work is in progress to test this hypothesis.…”

Polyamine-dependent gene expression

“…When DFMO is used to deplete the polyamines, there is a subsequent induction of COX-2 protein, with, however, only a minimal effect on COX-2 RNA levels [87]. The COX-2 3¢-untranslated region (UTR) contains sequences recognized by eIF5A, as reported by Xu and Chen [88].…”

“…The COX-2 3¢-untranslated region (UTR) contains sequences recognized by eIF5A, as reported by Xu and Chen [88]. Studies showed that the DFMO-dependent change in COX-2 protein was mimicked by the eIF5A response elements contained in the COX-2 RNA 3¢ UTR [87]. It has long been known that polyamines are necessary for stabilization and for crystallization of transfer RNAs (tRNAs) [89,90].…”

Polyamines affect histamine synthesis during early stages of IL‐3‐induced bone marrow cell differentiation

“…For example, both spermine and-to a lesser extent-spermidine inhibit the activation and production of cytokines like TNF by the macrophagelike cell line RAW 264.7 [Zhang et al, 1997], inhibit the secretion of TNFa and MCP-1 in LPS-stimulated NR8383 macrophages [PerezCano et al, 2003], and cause loss of the innate immune response to Helicobacter pylori by inhibition of inducible nitric-oxide synthase translation [Bussiere et al, 2005]. Furthermore, it has been shown that spermine prevents macrophage differentiation from the human myeloid leukemia HL-60 cells [Gavin et al, 2004], and inhibition of polyamine biosynthesis by DFMO enhances nitric oxide production in LPS-activated J774 macrophages [Baydoun and Morgan, 1998] and upregulates COX-2 mRNA levels in Caco-2 human colon adenocarcinoma cells [Parker and Gerner, 2002]. All these inhibitory roles of polyamines, together with the fact that they are accumulated at the inflammation sites as a consequence of tissue regeneration and cell damage, support the hypothesis proposed by Zhang et al [2000] that extracellular polyamine levels could constitute a signal to prevent the tissue damage provoked by an excessive inflammatory response [Zhang et al, 2000].…”