2008
DOI: 10.1002/hep.22231
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S-adenosylmethionine inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation

Abstract: We previously showed that S-adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)-induced tumor necrosis factor ␣ (TNF␣) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcriptional level without affecting nuclear factor B nuclear binding. However, the exact molecular mechanism or mechanisms of the inhibitory effect were unclear. While SAMe is a methyl donor, MTA is an inhibitor of methylation. SAMe can convert to MTA spontaneously, … Show more

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Cited by 96 publications
(97 citation statements)
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“…Because AdoMet is a universal methyl donor, the increase in the concentration of intracellular AdoMet might result in imbalances in methylation or post-translational modification of proteins in the ER. It has also been reported that AdoMet inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation (75). Because AdoMet is involved in multiple pathways, it is possible that under these experimental conditions AdoMet induces ER stress via pathways that are independent of homocysteine.…”
Section: Discussionmentioning
confidence: 99%
“…Because AdoMet is a universal methyl donor, the increase in the concentration of intracellular AdoMet might result in imbalances in methylation or post-translational modification of proteins in the ER. It has also been reported that AdoMet inhibits lipopolysaccharide-induced gene expression via modulation of histone methylation (75). Because AdoMet is involved in multiple pathways, it is possible that under these experimental conditions AdoMet induces ER stress via pathways that are independent of homocysteine.…”
Section: Discussionmentioning
confidence: 99%
“…It is speculated that SAMe is unstable, whereas methylthioadenosine (MTA) derived from SAMe is not [9]. Treatment with SAMe doubles MTA and S-adenosyl-homocysteine (SAH) levels [9].…”
Section: Discussionmentioning
confidence: 99%
“…It is speculated that SAMe is unstable, whereas methylthioadenosine (MTA) derived from SAMe is not [9]. Treatment with SAMe doubles MTA and S-adenosyl-homocysteine (SAH) levels [9]. In vitro studies, where RAW cells were treated with different doses of SAMe, increased the levels of SAMe, MTA, and SAH in a dose dependent manner [9].…”
Section: Discussionmentioning
confidence: 99%
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