17A, a novel non-coding RNA, regulates GABA B alternative splicing and signaling in response to inflammatory stimuli and in Alzheimer disease

Massone, Sara; Vassallo, Irene; Fiorino, Gloria; Castelnuovo, Manuele; Barbieri, Federica; Borghi, Roberta; Tabaton, Massimo; Robello, Mauro; Gatta, Elena; Russo, Claudio; Florio, Tullio; Dieci, Giorgio; Cancedda, Ranieri; Pagano, Aldo

doi:10.1016/j.nbd.2010.09.019

Cited by 214 publications

(154 citation statements)

References 19 publications

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“…In this study, we used SH-SY5Y cells since they are human neuronal cells that endogenously express MORs as well as GABA and NMDA receptors (14)(15)(16), making them an excellent tool for an in vitro study concerning propofol's effects on MOR expression and the underlying molecular mechanisms. Based on our findings, it would be of note to identify signaling pathways involved in the propofol-induced transcriptional regulation of the MOR gene in future studies.…”

Section: Discussionmentioning

confidence: 99%

Propofol increases μ-opioid receptor expression in SH-SY5Y human neuroblastoma cells

Pei

Cao

et al. 2012

Molecular Medicine Reports

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Abstract. The aim of the present study was to explore the effect of propofol, a intravenous sedative-hypnotic agent used widely in inducing and maintaining anesthesia, on µ-opioid receptor (MOR) expression in a human neuronal cell line. SH-SY5Y human neuroblastoma cells were treated with various concentrations of propofol (1, 5, 10 or 20 µM) for different lengths of time (6, 12 or 24 h). Real-time quantitative RT-PCR showed that at a concentration range of 1-10 µM, propofol increased MOR mRNA levels in a statistically significant dose-and time-dependent manner within 12 h of treatment. Western blot analyses demonstrated that propofol treatment for 12 h dosedependently increased the MOR protein levels. In the 12-h SH-SY5Y-treated cells, propofol dose-dependently increased MOR density (B max ) in the cell membranes. In addition, in the presence of the transcription inhibitor actinomycin D (1 mg/ml), propofol (10 µM) had no significant effect on the MOR mRNA levels over time. The results suggested that propofol dose-and time-dependently enhances MOR expression in SH-SY5Y human neuroblastoma cells at the transcriptional level, leading to an increased density of ligand-binding MORs in the cell membranes. This study demonstrated for the first time a link between propofol and the opioid system, thereby providing new insights into propofol mechanism of action and potential for abuse.

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Section: Discussionmentioning

confidence: 99%

Propofol increases μ-opioid receptor expression in SH-SY5Y human neuroblastoma cells

Pei

Cao

et al. 2012

Molecular Medicine Reports

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“…Although the mode of action of such deregulated lncRNAs is mainly unknown so far, it will be interesting to test whether such lncRNAs may serve as disease-specific biomarkers for AD. The expression of three specific lncRNAs, 17A, NDM29 and 51A was reported to be upregulated in AD affected brains compared to healthy control brain tissues [60][61][62]. The lncnRNA 17A, embedded in an antisense orientation in the third intron of the human G-protein-coupled receptor 51 (GPR51, also known as GABBR2) gene, was demonstrated to regulate GPR51/GABBR2 pre-mRNA processing and favour the generation of the alternative and unfunctional splicing isoform B of the GABA B receptor (GABAB R2) ( Figure 2) [60].…”

Section: Alzheimer Diseasementioning

confidence: 99%

“…The expression of three specific lncRNAs, 17A, NDM29 and 51A was reported to be upregulated in AD affected brains compared to healthy control brain tissues [60][61][62]. The lncnRNA 17A, embedded in an antisense orientation in the third intron of the human G-protein-coupled receptor 51 (GPR51, also known as GABBR2) gene, was demonstrated to regulate GPR51/GABBR2 pre-mRNA processing and favour the generation of the alternative and unfunctional splicing isoform B of the GABA B receptor (GABAB R2) ( Figure 2) [60]. Indeed, the stable expression of 17A in human neuroblastoma cells was shown to increase the synthesis of the GABAB R2 splicing isoform B that is defective of the intramembrane sequence peptide, thus generating non functional receptors unable to transduce GABAB-dependent intracellular signalling.…”

Section: Alzheimer Diseasementioning

confidence: 99%

The Long Non-Coding RNAs in Neurodegenerative Diseases: Novel Mechanisms of Pathogenesis

Riva¹,

Ratti²,

Venturin³

2016

CAR

271

167

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“…2 In the recent years we defined the transcriptional role of several of these ncRNA. [13][14][15][16][17][18][19] While investigating the biological role of one of these transcription units (named 21A), we documented an inverse correlation between the expression level of 21A ncRNA and the rate of cell proliferation. 2 Indeed, the transfection of cells with a construct expressing 21A ncRNA in antisense configuration led to a marked increase of cell proliferation.…”

Section: Introductionmentioning

confidence: 90%

Down-regulation of 21A Alu RNA as a tool to boost proliferation maintaining the tissue regeneration potential of progenitor cells

et al. 2016

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ABSTRACT21A is an Alu non-coding (nc) RNA transcribed by RNA polymerase (pol) III. While investigating the biological role of 21A ncRNA we documented an inverse correlation between its expression level and the rate of cell proliferation. The downregulation of this ncRNA not only caused a boost in cell proliferation, but was also associated to a transient cell dedifferentiation, suggesting a possible involvement of this RNA in cell dedifferentiation/reprogramming. In this study, we explored the possibility to enhance proliferation and dedifferentiation of cells of interest, by 21A down-regulation, using a mixture of chemically modified Anti-21A RNAs. Our results confirmed the validity of this approach that allows the amplification of specific cell populations, in a controlled manner and without inducing permanent effects. In addition to induce cell proliferation, the procedure did not decrease the tissue regeneration potential of progenitor cells in two different cell systems.

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17A, a novel non-coding RNA, regulates GABA B alternative splicing and signaling in response to inflammatory stimuli and in Alzheimer disease

Cited by 214 publications

References 19 publications

Propofol increases μ-opioid receptor expression in SH-SY5Y human neuroblastoma cells

Propofol increases μ-opioid receptor expression in SH-SY5Y human neuroblastoma cells

The Long Non-Coding RNAs in Neurodegenerative Diseases: Novel Mechanisms of Pathogenesis

Down-regulation of 21A Alu RNA as a tool to boost proliferation maintaining the tissue regeneration potential of progenitor cells

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