HDAC inhibitors TSA and sodium butyrate enhanced the human IL-5 expression by altering histone acetylation status at its promoter region

Han, ShouWei; Lü, Jun; Zhang, Yu; Cao, Cheng; Lin, Lynlee L.; Han, Liping; Huang, Baiqu

doi:10.1016/j.imlet.2006.12.001

Cited by 34 publications

(23 citation statements)

References 31 publications

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“…31 However, TSA alone had little effect on Il4 and Il13 mRNA (Fig 2, A) and no effect on IL-5 or IL-13 protein production (data not shown). This suggests that in the presence of PHA stimulation, TSA-mediated increases in T H 2-associated cytokine expression (Fig 2) are the result of both increased histone acetylation at Il4, Il5, and Il13 loci and enhanced expression of a T H 2-positive regulator or regulators.…”

Section: Inhibition Of Histone Deacetylase Activity Augments T H 2 Bumentioning

confidence: 82%

Epigenetic regulation of established human type 1 versus type 2 cytokine responses

Becker

Kozyrskyj

et al. 2008

Journal of Allergy and Clinical Immunology

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Section: Inhibition Of Histone Deacetylase Activity Augments T H 2 Bumentioning

confidence: 82%

Epigenetic regulation of established human type 1 versus type 2 cytokine responses

Becker

Kozyrskyj

et al. 2008

Journal of Allergy and Clinical Immunology

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“…While several locus-specific studies have linked HDACiinduced gene expression changes with corresponding increases in promoter histone acetylation (64,129,160), ChIP-seq studies suggest that the majority of promoters hyper-acetylated by HDACi do not undergo corresponding gene expression changes. These findings indicate that promoter acetylation alone is not sufficient to alter transcription (46).…”

Section: Hdaci-induced Histone Acetylation and Corresponding Changes mentioning

confidence: 99%

Mechanisms of Histone Deacetylase Inhibitor-Regulated Gene Expression in Cancer Cells

Chüeh

Tse

Tögel

et al. 2015

Antioxidants & Redox Signaling

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Significance: Class I and II histone deacetylase inhibitors (HDACis) are approved for the treatment of cutaneous T-cell lymphoma and are undergoing clinical trials as single agents, and in combination, for other hematological and solid tumors. Understanding their mechanisms of action is essential for their more effective clinical use, and broadening their clinical potential. Recent Advances: HDACi induce extensive transcriptional changes in tumor cells by activating and repressing similar numbers of genes. These transcriptional changes mediate, at least in part, HDACi-mediated growth inhibition, apoptosis, and differentiation. Here, we highlight two fundamental mechanisms by which HDACi regulate gene expression-histone and transcription factor acetylation. We also review the transcriptional responses invoked by HDACi, and compare these effects within and across tumor types. Critical Issues: The mechanistic basis for how HDACi activate, and in particular repress gene expression, is not well understood. In addition, whether subsets of genes are reproducibly regulated by these agents both within and across tumor types has not been systematically addressed. A detailed understanding of the transcriptional changes elicited by HDACi in various tumor types, and the mechanistic basis for these effects, may provide insights into the specificity of these drugs for transformed cells and specific tumor types. Future Directions: Understanding the mechanisms by which HDACi regulate gene expression and an appreciation of their transcriptional targets could facilitate the ongoing clinical development of these emerging therapeutics. In particular, this knowledge could inform the design of rational drug combinations involving HDACi, and facilitate the identification of mechanism-based biomarkers of response. Antioxid. Redox Signal. 23, 66-84.

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“…It was also shown that the complex mechanism of acetylation and deacetylation can modulate NF-kB transcriptional activity via proteins in the NF-kB pathway as well as in modulating the accessibility of the NF-kB target genes [64]. IL-5, a typical T H 2 cytokine, is upregulated by butyrate-induced acetylation at its promoter site [65]. Butyrate and propionate repress LPS-induced TNF-a expression by upregulation of PGE 2 and cycloogygenase 2 (COX-2) via inhibition of HDAC in PBMCs and RAW 264.7 [40 ,56,66].…”

Section: Mechanisms Of Butyrate-modulated Cytokine Expressionmentioning

confidence: 99%

Butyrate and other short-chain fatty acids as modulators of immunity: what relevance for health?

Meijer¹,

Vos

Priebe³

2010

Current Opinion in Clinical Nutrition and Metabolic Care

385

259

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SCFAs show anti-inflammatory effects and seem to have the potency to prevent infiltration of immune cells from the bloodstream in, for example, the adipose tissue. In addition, their ability to inhibit the proliferation and activation of T cells and to prevent adhesion of antigen-presenting cells could be important as it recently has been shown that obesity-associated inflammation might be antigen-dependent. More studies with concentrations in micromolar range are needed to approach more physiological concentrations.

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HDAC inhibitors TSA and sodium butyrate enhanced the human IL-5 expression by altering histone acetylation status at its promoter region

Cited by 34 publications

References 31 publications

Epigenetic regulation of established human type 1 versus type 2 cytokine responses

Epigenetic regulation of established human type 1 versus type 2 cytokine responses

Mechanisms of Histone Deacetylase Inhibitor-Regulated Gene Expression in Cancer Cells

Butyrate and other short-chain fatty acids as modulators of immunity: what relevance for health?

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