Neuron-restrictive silencer factor causes epigenetic silencing of Kv4.3 gene after peripheral nerve injury

Uchida, Hitoshi; Sasaki, Keita; Ma, Lin; Ueda, Hiroshi

doi:10.1016/j.neuroscience.2009.12.021

Cited by 86 publications

(80 citation statements)

References 18 publications

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“…These suppressors play important roles in repressing ion channel expression. Indeed, p53 negatively regulates the voltage-gated K 1 channel EAG-1 (ether á go-go-1 K 1 channel) (Lin et al, 2011), and repressor element 1-silencing transcription factor negatively regulates the voltage-gated K 1 channel K V 4.3 and Ca 21 -activated K 1 channel K Ca 3.1 in several different types of cells, including cancer cells (Cheong et al, 2005;Uchida et al, 2010;Ohya et al, 2011). HDAC3 selectively binds to many types of transcriptional repressors.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Ca²⁺-Activated Cl⁻ Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells

Matsuba

Niwa

Muraki

et al. 2014

J Pharmacol Exp Ther

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The Ca 21 -activated Cl 2 channel transmembrane proteins with unknown function 16 A (TMEM16A; also known as anoctamin 1 or discovered on gastrointestinal stromal tumor 1) plays an important role in facilitating the cell growth and metastasis of TMEM16A-expressing cancer cells. Histone deacetylase (HDAC) inhibitors (HDACi) are useful agents for cancer therapy, but it remains unclear whether ion channels are epigenetically regulated by them. Using real-time polymerase chain reaction, Western blot analysis, and whole-cell patch-clamp assays, we found a significant decrease in TMEM16A expression and its functional activity was induced by the vorinostat, a pan-HDACi in TMEM16A-expressing human cancer cell lines, the prostatic cancer cell line PC-3, and the breast cancer cell line YMB-1. TMEM16A downregulation was not induced by the chemotherapy drug paclitaxel in either cell

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Section: Discussionmentioning

confidence: 99%

Downregulation of Ca²⁺-Activated Cl⁻ Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells

Matsuba

Niwa

Muraki

et al. 2014

J Pharmacol Exp Ther

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“…Indeed, nerve injuries such as optic nerve injury and hypoglossal nerve injury enhance the expression of HDAC family proteins (Pelzel et al, 2010) and our unpublished data. Neuron-restrictive silencer factor (NRSF) is up-regulated after sciatic nerve injury and recruits HDACs to suppress the expression of Nav1.8 sodium channels, u-opioid receptor (MOP) and the voltage-gated potassium channel Kv4.3 in injured DRG neurons (Uchida et al, 2010a, b). Usually, NRSF represses the expression of neuronal genes in non-neuronal cells, although it can be an activator in some situations (Ballas et al, 2005).…”

Section: Potential Involvement Of Epigenetic Modificationmentioning

confidence: 99%

The nuclear events guiding successful nerve regeneration

Kiryu‐Seo¹,

Kiyama²

2011

Front. Mol. Neurosci.

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Peripheral nervous system (PNS) neurons survive and regenerate after nerve injury, whereas central nervous system (CNS) neurons lack the capacity to do so. The inability of the CNS to regenerate presumably results from a lack of intrinsic growth activity and a permissive environment. To achieve CNS regeneration, we can learn from successful nerve regeneration in the PNS. Neurons in the PNS elicit dynamic changes in gene expression in response to permissive environmental cues following nerve injury. To switch gene expression on and off in injured neurons, transcription factors and their networks should be carefully orchestrated according to the regeneration program. This is the so-called “intrinsic power of axonal growth.” There is an increasing repertoire of candidate transcription factors induced by nerve injury. Some of them potentiate the survival and axonal regeneration of damaged neurons in vivo; however, our knowledge of transcriptional events in injured neurons is still limited. How do these transcription factors communicate with each other? How does the transcriptional machinery regulate the wide variety of regeneration-associated genes (RAGs) in the properly coordinated manner? In this review, we describe our current understanding of the injury-inducible transcriptional factors that enhance the intrinsic growth capacity, and propose a potential role for specificity protein 1 (Sp1), which provides a platform to recruit injury-inducible transcription factors, in simultaneous gene regulation. Finally, we discuss an additional mechanism that is involved in epigenetic modifications in damaged neurons. A comprehensive understanding of the nuclear events in injured neurons will provide clues to clinical interventions for successful nerve regeneration.

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“…Interestingly, results of immunohistochemistry indicated that most upregulated REST were in DRG neurons rather than in non-neuronal cells as found by others previously [163]. They identified that upregulated REST interacted with its cis -element RE-1 (or NRSE) in the promoters of OPRM1 , Nav1.8 and Kv4.3 [161–162]. They showed that the binding was responsible for the downregulation of their mRNAs in the injured DRGs since downregulation of REST by antisense oligonucleotide restored expression of these mRNAs.…”

Section: Introductionmentioning

confidence: 66%

“…Initially, they found that PSL mice in their DRG upregulated mRNA of transcription factor REST (or NRSF) from its promoter II being associated with an increase in acetylated H4 (acH4), but not acH3, to this promoter at least 7 days after nerve injury [161–162]. Interestingly, results of immunohistochemistry indicated that most upregulated REST were in DRG neurons rather than in non-neuronal cells as found by others previously [163].…”

Section: Introductionmentioning

confidence: 88%

Epigenetic regulation of persistent pain

Bai

Ren

Dubner

2015

Translational Research

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Persistent or chronic pain is tightly associated with various environmental changes and linked to abnormal gene expression within cells processing nociceptive signaling. Epigenetic regulation governs gene expression in response to environmental cues. Recent animal model and clinical studies indicate that epigenetic regulation plays an important role in the development/maintenance of persistent pain and, possibly the transition of acute pain to chronic pain, thus shedding light in a direction for development of new therapeutics for persistent pain.

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Neuron-restrictive silencer factor causes epigenetic silencing of Kv4.3 gene after peripheral nerve injury

Cited by 86 publications

References 18 publications

Downregulation of Ca²⁺-Activated Cl⁻ Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells

Downregulation of Ca²⁺-Activated Cl⁻ Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells

The nuclear events guiding successful nerve regeneration

Epigenetic regulation of persistent pain

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Neuron-restrictive silencer factor causes epigenetic silencing of Kv4.3 gene after peripheral nerve injury

Cited by 86 publications

References 18 publications

Downregulation of Ca2+-Activated Cl− Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells

Downregulation of Ca2+-Activated Cl− Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells

The nuclear events guiding successful nerve regeneration

Epigenetic regulation of persistent pain

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Product

Resources

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Downregulation of Ca²⁺-Activated Cl⁻ Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells

Downregulation of Ca²⁺-Activated Cl⁻ Channel TMEM16A by the Inhibition of Histone Deacetylase in TMEM16A-Expressing Cancer Cells