Inhibition of interleukin-13 gene expression in T cells through GATA-3 pathway by arsenic trioxide

Yao, Xin; He, Hui; Yang, Yan; Dai, Shanlin; Sun, Ping; Kai-sheng, Yin; Huang, Mao Hsuan

doi:10.1097/00029330-200811020-00024

Cited by 3 publications

(2 citation statements)

References 6 publications

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“…The putative transcription factor binding sites include hepatocyte nuclear factor (HNF), CCAAT-enhancer binding protein (C/EBP), GATA-1, -2–3, Sp1, transcription factor family E2F and homeobox protein NKX2. Interestingly, in previous studies, inorganic arsenic altered expression of C/EBP (Lin et al, 2005), SP1 (Jutooru et al, 2010), GATA -3 (Yao et al, 2008) and E2F (Yamamoto et al, 2008). Nevertheless, how site-specific methylation of AS3MT contributes to the binding with these transcription factors needs further investigation.…”

Section: Discussionmentioning

confidence: 81%

Differential methylation of the arsenic (III) methyltransferase promoter according to arsenic exposure

et al. 2013

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Inorganic arsenic is methylated in the body by arsenic (III) methyltransferase. Arsenic methylation is thought to play a role in arsenic-related epigenetic phenomena including aberrant DNA and histone methylation. However, it is unclear whether the promoter of the AS3MT gene, which codes for arsenic (III) methyltransferase, is differentially methylated as a function of arsenic exposure. In this study we evaluated AS3MT promoter methylation according to exposure, assessed by urinary arsenic excretion in a stratified random sample of 48 participants from the Strong Heart Study who had urine arsenic measured at baseline and DNA available from 1989–1991 and 1998–1999. For this study, all data are from the 1989–1991 visit. We measured AS3MT promoter methylation at its 48 CpG loci by bisulphite sequencing. We compared mean % methylation at each CpG locus by arsenic exposure group using linear regression adjusted for study centre, age and sex. A hypomethylated region in the AS3MT promoter was associated with higher arsenic exposure. In vitro, arsenic induced AS3MT promoter hypomethylation and it increased AS3MT expression in human peripheral blood mononuclear cells. These findings may suggest that arsenic exposure influences the epigenetic regulation of a major arsenic metabolism gene.

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Section: Discussionmentioning

confidence: 81%

Differential methylation of the arsenic (III) methyltransferase promoter according to arsenic exposure

et al. 2013

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“…IL‐13 is a crucial mediator of allergic inflammation and produced by Th2, BSMC, and other cells. While GATA‐3 acts as a transcription factor, regulating Th2 differentiation and IL‐13 expression [Zhu et al, 2006; Yao et al, 2008], little is known whether other factors could modulate IL‐13 secretion. In this study, we attempted to identify the proteins interacted with IL‐13 and their regulatory roles in the expression and secretion of IL‐13 in both human BSMC and lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

SUMF2 interacts with interleukin‐13 and inhibits interleukin‐13 secretion in bronchial smooth muscle cells

Liang

et al. 2009

J of Cellular Biochemistry

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IL-13 is a central mediator of allergic inflammation and secreted by Th2 and bronchial smooth muscle cells (BSMC). However, little is known about the regulation of IL-13 secretion. To address it, a cDNA library of BSMC was screened for the proteins interacted with IL-13 by yeast two-hybridization. Besides IL-13 receptors, human sulfatase modifying factor 2 (SUMF2) was interacted with IL-13. Furthermore, SUMF2 and IL-13 were co-immunoprecipitated from BSMC, which was independent of IL-13 glycosylation. Interestingly, high levels of SUMF2 were expressed by BSMC, accompanied by significantly higher levels of intracellular IL-13, but lower levels of IL-13 secretion from BSMC. In contrast, little of SUMF2 was detected in lymphocytes, accompanied by lower levels of intracellular IL-13, but significantly higher levels of 12 kDa form of IL-13 secretion. Moreover, knockdown of SUMF2 expression by transfection with SUMF2-specific siRNA did not alter IL-13 mRNA transcription, but significantly reduced intracellular IL-13 levels, associated with increased levels of IL-13 secretion from BSMC. While induction of transient SUMF2 expression in lymphocytes failed to modulate IL-13 mRNA transcription. It significantly increased the contents of 12 kDa form of intracellular IL-13, accompanied by significantly reduced levels of IL-13 in their supernatants. In addition, blockage of N-glycosylation by treatment with tunicamycin eliminated 17 kDa form of intracellular IL-13, but failed to promote IL-13 secretion in BSMC. Collectively, our novel data clearly indicated that SUMF2 interacted with IL-13 and inhibited IL-13 secretion in BSMC and lymphocytes, which was independent of IL-13 glycosylation.

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Importins and Exportins Regulating Allergic Immune Responses

Aggarwal

Agrawal

2014

Mediators of Inflammation

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Nucleocytoplasmic shuttling of macromolecules is a well-controlled process involving importins and exportins. These karyopherins recognize and bind to receptor-mediated intracellular signals through specific signal sequences that are present on cargo proteins and transport into and out of the nucleus through nuclear pore complexes. Nuclear localization signals (NLS) present on cargo molecules to be imported while nuclear export signals (NES) on the molecules to be exported are recognized by importins and exportins, respectively. The classical NLS are found on many transcription factors and molecules that are involved in the pathogenesis of allergic diseases. In addition, several immune modulators, including corticosteroids and vitamin D, elicit their cellular responses by regulating the expression and activity of importin molecules. In this review article, we provide a comprehensive list of importin and exportin molecules and their specific cargo that shuttled between cytoplasm and the nucleus. We also critically review the role and regulation of specific importin and exportin involved in the transport of activated transcription factors in allergic diseases, the underlying molecular mechanisms, and the potential target sites for developing better therapeutic approaches.

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Inhibition of interleukin-13 gene expression in T cells through GATA-3 pathway by arsenic trioxide

Cited by 3 publications

References 6 publications

Differential methylation of the arsenic (III) methyltransferase promoter according to arsenic exposure

Differential methylation of the arsenic (III) methyltransferase promoter according to arsenic exposure

SUMF2 interacts with interleukin‐13 and inhibits interleukin‐13 secretion in bronchial smooth muscle cells

Importins and Exportins Regulating Allergic Immune Responses

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