An updated role of microRNA-124 in central nervous system disorders: a review

Sun, Yang; Luo, Zhu-Min; Guo, Xiu-Ming; Su, Ding‐Feng; Liu, Xia

doi:10.3389/fncel.2015.00193

Cited by 188 publications

(166 citation statements)

References 85 publications

(103 reference statements)

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“…Significant decrease of miR-124 was described in the SN of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice (PD mouse model) as well as in MN9D dopaminergic neurons treated with methyl phenyl pyridinium (MPP) iodide, while its overexpression improved cell survival [20,21]. Therefore, increasing miR-124 intracellular levels likely stands for a novel therapeutic strategy to improve functional outcome in PD (reviewed by Sun et al 2015 [3]). …”

Section: Introductionmentioning

confidence: 99%

“…In rodents, newborn neurons generated in the SVZ migrate through the rostral migratory stream (RMS) towards the olfactory bulb (OB) where they fully differentiate as mature interneurons [2]. Adult neurogenesis homeostasis is altered in several brain disorders including Parkinson's disease (PD) [3]. PD is characterized by the loss of dopaminergic (DA) neurons present in the substantia nigra (SN) and degeneration of DA terminals in the striatum, leading to movement coordination impairments and cognitive deficits.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Saraiva

Paiva

Santos

et al. 2016

Journal of Controlled Release

142

128

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Modulation of the subventricular zone (SVZ) neurogenic niche can enhance brain repair in several disorders including Parkinson's disease (PD). Herein, we used biocompatible and traceable polymeric nanoparticles (NPs) containing perfluoro-1,5-crown ether (PFCE) and coated with protamine sulfate to complex microRNA-124 (miR-124), a neuronal fate determinant. The ability of NPs to efficiently deliver miR-124 and prompt SVZ neurogenesis and brain repair in PD was evaluated. In vitro, miR-124 NPs were efficiently internalized by neural stem/progenitors cells and neuroblasts and promoted their neuronal commitment and maturation. The expression of Sox9 and Jagged1, two miR-124 targets and stemness-related genes, were also decreased upon miR-124 NP treatment. In vivo, the intracerebral administration of miR-124 NPs increased the number of migrating neuroblasts that reached the granule cell layer of the olfactory bulb, both in healthy and in a 6-hydroxydopamine (6-OHDA) mouse model for PD.MiR-124 NPs were also able to induce migration of neurons into the lesioned striatum of 6-OHDA-treated mice. Most importantly, miR-124 NPs proved to ameliorate motor symptoms of 6-OHDA mice, monitored by the apomorphine-induced rotation test.Altogether, we provide clear evidences to support the use of miR-124 NPs as a new therapeutic approach to boost endogenous brain repair mechanisms in a setting of neurodegeneration.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Saraiva

Paiva

Santos

et al. 2016

Journal of Controlled Release

142

128

View full text Add to dashboard Cite

show abstract

“…MiR-124 is the most abundant miRNA in the brain. It plays numerous roles in neuronal proliferation, apoptosis and cell death, and has been proposed as a marker of brain damage after stroke and cardiac arrest in adults [12,13]. MiR-125b is highly enriched in the brain and has been put forward as a potential marker of acute stroke in adults [11,14].…”

Section: Introductionmentioning

confidence: 99%

Temporal Profile of Circulating microRNAs after Global Hypoxia-Ischemia in Newborn Piglets

Garberg¹,

Huun²,

Baumbusch³

et al. 2016

Neonatology

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Background: There is a lack of reliable biomarkers that can identify and grade acute hypoxic-ischemic encephalopathy in newborns. MicroRNAs (miRNA) are short, non-coding strands of RNA that are released into the circulation in response to tissue stress and injury. Some miRNAs are highly tissue specific and thus may potentially be non-invasive biomarkers of neonatal hypoxic-ischemic brain injury. Objective: The aim of this study was to characterize the temporal expression of selected circulating miRNAs in a clinically relevant piglet model of neonatal hypoxia-ischemia (HI). Methods: A total of 13 anesthetized newborn piglets were randomized to either a control group (n = 5) or transient global HI group (n = 8). HI was achieved by ventilation with 8% oxygen until the point of severe acidosis (arterial base excess ≤-20 mmol/l) and/or hypotension (mean arterial blood pressure ≤20 mm Hg) was reached. Plasma was sampled at baseline, at the end of HI and 0.5, 3.5 and 9.5 h after HI. MiRNA expression was measured by qRT-PCR. Results: Compared to baseline, miR-374a increased during HI (p = 0.01), remained elevated at 0.5 h after HI (p = 0.02) and was downregulated at 9.5 h after HI (p = 0.02). MiR-210 increased during HI (p = 0.02) and rapidly normalized by 0.5 h after HI. MiR-124 and miR-125b did not exhibit significant alterations. Correlations were observed between miR-374a, arterial pH, base excess and lactate levels, and between miR-210 and pO₂ (p < 0.05). Conclusions: Our data suggest that miR-374a and miR-210 are important regulators in neonatal HI and might have a place as biomarkers in this setting.

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“…miRNA-124 is abundantly and specifically expressed in the brain, but is expressed at a low level in other tissues (5); it has a critical role in central nervous system development and function, as well as the progression of various diseases in brain (5). Recently, miR-124 has been found down-regulated in multiple tumor types, including cancer (6), prostate (7), lung (8) and colorectal cancer (9).…”

Section: Introductionmentioning

confidence: 99%

Lentivirus-mediated overexpression of miR-124 suppresses growth and invasion by targeting JAG1 and EZH2 in gastric cancer

Chen

et al. 2018

Oncol Lett

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Abstract. expression is downregulated and has a tumor suppressor role in various types of cancer. The present study revealed that genes encoding miR-124 were frequently methylated and the expression of miR-124 was downregulated in gastric cancer tissues. Stable expression of miR-124 using a lentiviral vector inhibited gastric cancer cell growth, migration and invasion in vitro. In addition, overexpression of miR-124 suppressed gastric cancer cell xenograft growth in nude mice. The expression of the Notch ligand Jagged1 (JAG1) and enhancer of zeste homolog 2 (EZH2) was downregulated upon miR-124 overexpression, and silencing of JAG1 or EZH2 by RNA interference also suppressed gastric cancer cell growth, migration and invasion. Furthermore, expression of fibronectin and vimentin, not able elements of the epithelial-mesenchymal transition, were suppressed by overexpression of miR-124 or inhibition of JAG1 or EZH2 expressions in GC. Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.

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An updated role of microRNA-124 in central nervous system disorders: a review

Cited by 188 publications

References 85 publications

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease

Temporal Profile of Circulating microRNAs after Global Hypoxia-Ischemia in Newborn Piglets

Lentivirus-mediated overexpression of miR-124 suppresses growth and invasion by targeting JAG1 and EZH2 in gastric cancer

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