Retinoic Acid-Induced Chromatin Remodeling of Mouse κ Opioid Receptor Gene

Park, Sung Wook; Huq, M. D. Mostaqul; Loh, Horace H.; Wei, Li‐Na

doi:10.1523/jneurosci.0186-05.2005

Cited by 35 publications

(49 citation statements)

References 31 publications

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“…This involves principally transcriptional events such as acquiring specific transcription factors and engaging in chromatin remodeling events (Park et al, 2005). Posttranscriptional regulation has been demonstrated for KOR, such as regulating its mRNA stability, transport, and translation Bi et al, 2003;Wei, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Regulation of their expression has been extensively examined, primarily at the level of gene transcription regulated by vitamin A, cytokines (Bi et al, 2001;Park et al, 2002;Wei and Loh, 2002;Hu et al, 2004), and specific transcription factors (Kraus et al, 2001;Kim et al, 2004). They also often involve chromatin remodeling events that occur over a period of time and are more permanent (Park et al, 2005). However, when a more rapid response in receptor expression is needed, it could become very inefficient by changing their transcriptional programs.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Netrin-1 Signaling RegulatesDe NovoProtein Synthesis of κ Opioid Receptor by Facilitating Polysomal Partition of Its mRNA

Tsai¹,

Bi²,

Loh³

et al. 2006

J. Neurosci.

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The expression of opioid receptor (KOR) is subjected to both transcriptional and posttranscriptional controls. We report that KOR translation is regulated by netrin-1 in primary neurons of dorsal root ganglion (DRG) and in P19 embryonal carcinoma cells. Without stimulation, a significant portion of KOR mRNA is maintained in a dormant state and partitions in the translationally inactive, postpolysomal fraction. During netrin-1 stimulation, which activates its downstream target focal adhesion kinase (FAK), KOR mRNA rapidly partitions to the translationally active polysomal fraction. Functionally, the newly synthesized KOR proteins in DRG neurons are able to bind to specific ligands. This report describes the first example of netrin-1 signaling in the translational control of a drug receptor KOR, which involves the mediator of netrin-1, FAK, and a novel mechanism that enhances the association of target mRNA with polysomes for translational activation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Netrin-1 Signaling RegulatesDe NovoProtein Synthesis of κ Opioid Receptor by Facilitating Polysomal Partition of Its mRNA

Tsai¹,

Bi²,

Loh³

et al. 2006

J. Neurosci.

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show abstract

“…A similar reaction was carried out using primers for ␤-actin (9) as an internal control, except the number of cycles was reduced to 20. Primers for ␦ (DOR) and (KOR) opioid receptors were as described previously (67,80). Primers for N-cadherin, ␤III-tubulin, and glial fibrillary acidic protein (GFAP) are described in Table 1.…”

Section: Rt-pcr and Real-time Quantitative Rt-pcr (Qrt-pcr)mentioning

confidence: 99%

Evidence of Endogenous Mu Opioid Receptor Regulation by Epigenetic Control of the Promoters

Hwang

Song

Kim

et al. 2007

Molecular and Cellular Biology

145

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The pharmacological effect of morphine as a painkiller is mediated mainly via the mu opioid receptor (MOR) and is dependent on the number of MORs in the cell surface membrane. While several studies have reported that the MOR gene is regulated by various cis-and trans-acting factors, many questions remain unanswered regarding in vivo regulation. The present study shows that epigenetic silencing and activation of the MOR gene are achieved through coordinated regulation at both the histone and DNA levels. In P19 mouse embryonal carcinoma cells, expression of the MOR was greatly increased after neuronal differentiation. MOR expression could also be induced by a demethylating agent (5-aza-2-deoxycytidine) or histone deacetylase inhibitors in the P19 cells, suggesting involvement of DNA methylation and histone deacetylation for MOR gene silencing. Analysis of CpG DNA methylation revealed that the proximal promoter region was unmethylated in differentiated cells compared to its hypermethylation in undifferentiated cells. In contrast, the methylation of other regions was not changed in either cell type. Similar methylation patterns were observed in the mouse brain. In vitro methylation of the MOR promoters suppressed promoter activity in the reporter assay. Upon differentiation, the in vivo interaction of MeCP2 was reduced in the MOR promoter region, coincident with histone modifications that are relevant to active transcription. When MeCP2 was disrupted using MeCP2 small interfering RNA, the endogenous MOR gene was increased. These data suggest that DNA methylation is closely linked to the MeCP2-mediated chromatin structure of the MOR gene. Here, we propose that an epigenetic mechanism consisting of DNA methylation and chromatin modification underlies the cell stage-specific mechanism of MOR gene expression.Opioids exert their pharmacological and physiological effects through binding to their endogenous receptors. Three types of opioid receptors, mu (), delta (␦), and kappa (), all belonging to the G-protein-coupled receptor superfamily, have been cloned. Upon agonist binding, these receptors couple to G proteins and affect several signal transduction pathways thought to mediate a broad range of functions and pharmacological effects of endogenous and exogenous opioids (51). Previous studies suggested that the opioid receptor (MOR) plays a key role in mediating the major clinical effects of analgesics, such as morphine, as well as the development of tolerance and physical dependence upon prolonged administration (39). MOR is mainly expressed in the central nervous system, with densities varying greatly in different regions, which can display different functional roles (55). During mouse embryonic development, the MOR message was specifically observed as early as embryonic day 8.5 (E8.5) using the reverse transcription (RT)-PCR method (44). In contrast, MOR transcripts were detected only beginning at E12 using the radioligand binding method (70) and at E10.5 by in situ hybridization (85). Transcript levels gradually incr...

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“…These PUVA-induced changes in epidermal innervation also have antipruritic effects, as shown by the use of anti-NGF or recombinant Sema3A replacement approaches against pruritus in atopic NC/Nga mice (Takano et al, 2005;Takano et al, 2007;Yamaguchi et al, 2008). Although the mechanisms by which PUVA influences expression of axonal guidance molecules remain unknown, treatment may affect chromatin remodeling and various transcription factors, such as activator protein-1 (AP-1) and poly(C) binding protein (Borner et al, 2002;Kim et al, 2004;Kim et al, 2005;Park et al, 2005). The NGF promoter contains an AP-1 element important for NGF transcriptional activity (Hengerer et al, 1990;D'Mello et al, 1991).…”

Section: Uv-based Therapy Of Ad Pruritus Involving Epidermal Hyperinnmentioning

confidence: 99%

Mechanisms Regulating Epidermal Innervation in Pruritus of Atopic Dermatitis

Tominaga¹,

Takamori²

2011

Skin Biopsy - Perspectives

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Retinoic Acid-Induced Chromatin Remodeling of Mouse κ Opioid Receptor Gene

Cited by 35 publications

References 31 publications

Netrin-1 Signaling RegulatesDe NovoProtein Synthesis of κ Opioid Receptor by Facilitating Polysomal Partition of Its mRNA

Netrin-1 Signaling RegulatesDe NovoProtein Synthesis of κ Opioid Receptor by Facilitating Polysomal Partition of Its mRNA

Evidence of Endogenous Mu Opioid Receptor Regulation by Epigenetic Control of the Promoters

Mechanisms Regulating Epidermal Innervation in Pruritus of Atopic Dermatitis

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