Publications by authors named "Annie Husson"
Article Synopsis
- Glutamine has an anti-inflammatory effect in the intestine via NF-κB transcription factor, reducing p65 protein levels in cell nuclei without affecting IL-1β stimulation.
- The study reveals that glutamine decreases NF-κB through the nuclear ubiquitin-proteasome pathway, involving the phosphorylation and degradation of IκBα and subsequent translocation of p65.
- Additionally, glutamine activates the IKKα subunit, which phosphorylates p65, leading to its degradation, with p38 MAPK serving as a mediator in this signaling pathway against inflammation.
Article Synopsis
- Amino acids like glutamine and arginine play crucial roles in regulating gene expression by activating specific signaling pathways and transcription factors.
- These amino acids have beneficial effects on intestinal health, promoting cell growth, reducing inflammation, and influencing metabolism through various mechanisms.
- While the role of transcription factors such as NF-kappaB and AP-1 in glutamine's functions is well-studied, the exact signaling pathways from amino acid entry into cells to gene activation remain largely unclear.
Article Synopsis
- Molecular data highlights various mechanisms by which amino acids regulate gene expression in mammalian cells, involving transcription factors and specific regulatory sequences.
- Glutamine, the most abundant amino acid, plays a crucial role in enhancing cell functions by activating various transcription factors linked to the inflammatory response, growth, and metabolic functions.
- Different signalling pathways, particularly involving kinases like mitogen-activated protein kinases, are suggested to mediate the effects of amino acids on transcription factors, though detailed pathways remain partially defined.
We previously demonstrated that the expression of the argininosuccinate synthetase (ASS) gene, a key step in nitric oxide production, is stimulated either by interleukin-1beta[Brasse-Lagnel et al. (2005) Biochimie 87, 403-9] or by glutamine in Caco-2 cells [Brasse-Lagnel et al. (2003) J.
View Article and Find Full Text PDFThe expression of the argininosuccinate synthetase gene (ASS), the limiting enzyme of arginine synthesis, was previously shown to be rapidly induced by a short-term (4 h) exposure to IL-1beta in Caco-2 cells [Biochimie, 2005, 403-409]. The present report shows that, by contrast, a long-term (24 h) exposure to IL-1beta inhibited the ASS activity despite an increase in both specific mRNA level and protein amount, demonstrating a post-translational effect. Concerning the mechanism involved, we demonstrate that the inhibiting effect is linked to the production of nitric oxide (NO) induced by IL-1beta.
View Article and Find Full Text PDFArgininosuccinate synthetase (ASS) is limiting the arginine synthesis and can be stimulated by immunostimulants. We previously identified a putative NF-kappaB element in the human ASS gene promoter but its functionality was unknown (Husson et al., Eur.
View Article and Find Full Text PDFHyper- (450 mOsm/l) and hypoosmotic exposure (150 mOsm/l) of Caco-2 cells, a human intestinal epithelial cell line, induced a twofold- and a fivefold increase in the production of IL-8, a constitutively expressed cytokine, respectively. This was observed both in the presence or in the absence of added proinflammatory cytokines and the stimulatory effect of osmotic stress was additive to that induced by the cytokines. Thus, IL-8 production appeared minimal around isoosmolarity, i.
View Article and Find Full Text PDFGlutamine stimulates the expression of the argininosuccinate synthetase (ASS) gene at both the level of enzyme activity and mRNA in Caco-2 cells. Searching to identify the pathway involved, we observed that (i) the stimulating effect of glutamine was totally mimicked by glucosamine addition, and (ii) its effect but not that of glucosamine was totally blocked by 6-diazo-5-oxo-l-norleucine (DON), an inhibitor of amidotransferases, suggesting that the metabolism of glutamine to glucosamine 6-phosphate was required. Moreover, run-on assays revealed that glucosamine was acting at a transcriptional level.
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