Transcription of the Tollip gene is elevated in intestinal epithelial cells through impaired O-GlcNAcylation-dependent nuclear translocation of the negative regulator Elf-1

Sugi, Yutaka; Takahashi, Kyôko; Nakano, Kou; Hosono, Akira; Kaminogawa, Shuichi

doi:10.1016/j.bbrc.2011.08.035

Cited by 18 publications

(16 citation statements)

References 21 publications

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“…A recent study found that Elf-1 suppressed the transcription of Tollip (18). Those previous findings prompted us to determine the effect of EGCG on nuclear Elf-1 expression based on immunofluorescence analysis, because Elf-1 had previously been shown to act as a repressor of nuclear Tollip expression (18). Our data demonstrated that treatment with 2.5 mM EGCG (45 min) promptly suppressed Elf-1 expression in mouse macrophages ( Fig.…”

Section: Egcg Suppresses Elf-1 Expression In Macrophagessupporting

confidence: 70%

“…Unlike other inflammation suppressors, little is known about the mechanism by which its expression is regulated. A recent study found that Elf-1 suppressed the transcription of Tollip (18). Those previous findings prompted us to determine the effect of EGCG on nuclear Elf-1 expression based on immunofluorescence analysis, because Elf-1 had previously been shown to act as a repressor of nuclear Tollip expression (18).…”

Section: Egcg Suppresses Elf-1 Expression In Macrophagesmentioning

confidence: 99%

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Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression

Kumazoe

Yamashita

Nakamura

et al. 2017

The Journal of Immunology

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TLR signaling is critical to innate immune system regulation; however, aberrant TLR signaling is involved in several diseases, including insulin resistance, Alzheimer's disease, and tumor metastasis. Moreover, a recent study found that TLR-4 signaling pathway inhibition might be a target for the suppression of chronic inflammatory disorders. In this article, we show that the green tea polyphenol epigallocatechin-3--gallate (EGCG) increases the expression of Toll interacting protein, a strong inhibitor of TLR4 signaling, by suppressing the expression of E74-like ETS transcription factor 1 (Elf-1). A mechanistic study revealed that EGCG suppressed Elf-1 expression via protein phosphatase 2A/cyclic GMP (cGMP)-dependent mechanisms. We also confirmed that orally administered EGCG and a cGMP inducer upregulated Toll interacting protein expression, increased intracellular levels of cGMP in macrophages, and suppressed Elf-1 expression. These data support EGCG and a cGMP inducer as potential candidate suppressors of TLR4 signaling.

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Section: Egcg Suppresses Elf-1 Expression In Macrophagessupporting

confidence: 70%

Section: Egcg Suppresses Elf-1 Expression In Macrophagesmentioning

confidence: 99%

Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression

Kumazoe

Yamashita

Nakamura

et al. 2017

The Journal of Immunology

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“…Each site constitutes a central motif in DNAse footprints obtained from CMP (mCD34), MEPs (CMK and K562 cells) or myelo-monocytic cells (CD14 + MNs, HL-60 and NB4). Both EGR1 and ELF1 can exert positive or negative regulatory effects on target gene expression in various myeloid lineages [79,80,81,82,83,84,85,86,87,88,89,90,91] so that either factor might inhibit full-length transcription of NRAMP1 in non-expressing cells (see Section 2.3.1.6). Lastly, transcriptional activity at DHS F10 was independently reported in K562 cells [49] thus supporting a regulatory role of this element in myeloid cells.…”

Section: Resultsmentioning

confidence: 99%

Developmental Control of NRAMP1 (SLC11A1) Expression in Professional Phagocytes

Cellier

2017

Biology

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NRAMP1 (SLC11A1) is a professional phagocyte membrane importer of divalent metals that contributes to iron recycling at homeostasis and to nutritional immunity against infection. Analyses of data generated by several consortia and additional studies were integrated to hypothesize mechanisms restricting NRAMP1 expression to mature phagocytes. Results from various epigenetic and transcriptomic approaches were collected for mesodermal and hematopoietic cell types and compiled for combined analysis with results of genetic studies associating single nucleotide polymorphisms (SNPs) with variations in NRAMP1 expression (eQTLs). Analyses establish that NRAMP1 is part of an autonomous topologically associated domain delimited by ubiquitous CCCTC-binding factor (CTCF) sites. NRAMP1 locus contains five regulatory regions: a predicted super-enhancer (S-E) key to phagocyte-specific expression; the proximal promoter; two intronic areas, including 3′ inhibitory elements that restrict expression during development; and a block of upstream sites possibly extending the S-E domain. Also the downstream region adjacent to the 3′ CTCF locus boundary may regulate expression during hematopoiesis. Mobilization of the locus 14 predicted transcriptional regulatory elements occurs in three steps, beginning with hematopoiesis; at the onset of myelopoiesis and through myelo-monocytic differentiation. Basal expression level in mature phagocytes is further influenced by genetic variation, tissue environment, and in response to infections that induce various epigenetic memories depending on microorganism nature. Constitutively associated transcription factors (TFs) include CCAAT enhancer binding protein beta (C/EBPb), purine rich DNA binding protein (PU.1), early growth response 2 (EGR2) and signal transducer and activator of transcription 1 (STAT1) while hypoxia-inducible factors (HIFs) and interferon regulatory factor 1 (IRF1) may stimulate iron acquisition in pro-inflammatory conditions. Mouse orthologous locus is generally conserved; chromatin patterns typify a de novo myelo-monocytic gene whose expression is tightly controlled by TFs Pu.1, C/ebps and Irf8; Irf3 and nuclear factor NF-kappa-B p 65 subunit (RelA) regulate expression in inflammatory conditions. Functional differences in the determinants identified at these orthologous loci imply that species-specific mechanisms control gene expression.

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“…In addition, SIGIRR, Tollip, and IRAK-M are also known to be expressed at high levels in IECs, and to thereby contribute to the hyporesponsiveness of IECs to commensals (64, 67, 68). Therefore, induction of these five negative regulators by bifidobacteria in BIE cells may be important for establishing tolerance against heat-stable ETEC MAMPs (Figure 2).…”

Section: Regulation Of Inflammation In Bie Cells By Immunobiotic Bifimentioning

confidence: 99%

Regulation of Toll-Like Receptors-Mediated Inflammation by Immunobiotics in Bovine Intestinal Epitheliocytes: Role of Signaling Pathways and Negative Regulators

2014

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Intestinal epithelial cells (IECs) detect bacterial and viral associated molecular patterns via germline-encoded pattern-recognition receptors (PRRs) and are responsible for maintaining immune tolerance to the communities of resident commensal bacteria while being also capable to mount immune responses against pathogens. Toll-like receptors (TLRs) are a major class of PRRs expressed on IECs and immune cells, which are involved in the induction of both tolerance and inflammation. In the last decade, experimental and clinical evidence was generated to support the application of probiotics with immunoregulatory capacities (immunobiotics) for the prevention and treatment of several gastrointestinal inflammatory disorders in which TLRs exert a significant role. The majority of these studies were performed in mouse and human cell lines, and despite the growing interest in the bovine immune system due to the economic importance of cattle as livestock, only few studies have been conducted on cattle. In this regard, our group has established a bovine intestinal epithelial (BIE) cell line originally derived from fetal bovine intestinal epitheliocytes and used this cell line to evaluate the impact of immunobiotics in TLR-mediated inflammation. This review aims to summarize the current knowledge of the beneficial effects of immunobiotics in the regulation of intestinal inflammation/infection in cattle. Especially, we discuss the role of TLRs and their negative regulators in both the inflammatory response and the beneficial effects of immunobiotics in bovine IECs. This review article emphasizes the cellular and molecular interactions of immunobiotics with BIE cells through TLRs and gives the scientific basis for the development of immunomodulatory feed for bovine healthy development.

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Transcription of the Tollip gene is elevated in intestinal epithelial cells through impaired O-GlcNAcylation-dependent nuclear translocation of the negative regulator Elf-1

Cited by 18 publications

References 21 publications

Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression

Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression

Developmental Control of NRAMP1 (SLC11A1) Expression in Professional Phagocytes

Regulation of Toll-Like Receptors-Mediated Inflammation by Immunobiotics in Bovine Intestinal Epitheliocytes: Role of Signaling Pathways and Negative Regulators

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