Increased striatal adenosine A2A receptor levels is an early event in Parkinson’s disease-related pathology and it is potentially regulated by miR-34b

Villar-Menéndez, Izaskun; Porta, Sílvia; Buira, Sandra Pérez; Pereira-Veiga, Thais; Díaz-Sánchez, Sara; Albasanz, José Luís; Ferrer, Isidre; Martı́n, Mairena; Barrachina, Marta

doi:10.1016/j.nbd.2014.05.030

Cited by 92 publications

(75 citation statements)

References 48 publications

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“…It is known that A 2A R expression is sensitive to hypoxia (Kobayashi and Millhorn, 1999), inflammation and other brain insults that can trigger up-regulation of the A 2A R in different brain regions (Chen et al, 2013;Chen et al, 2014). Indeed, the A 2A R up-regulation has been documented in human brains of early PD (Villar-Menendez et al, 2014) and AD (Albasanz et al, 2008;Orr et al, 2015), and animal models of PD (Yu et al, 2008), AD (Orr et al, 2015), HD (Li et al, 2015b), amyotrophic lateral sclerosis (Ng et al, 2015), attention deficit hyperactivity disorder (Pandolfo et al, 2013), chronic unpredictable stress (Kaster et al, 2015). Notably, the upregulation of the A 2A R in disease models were demonstrated in neuronal (particularly the nerve terminals) (Kaster et al, 2015;Li et al, 2015b) and some glial elements (Orr et al, 2015;Yu et al, 2008).…”

Section: Syn Fibrils Into Non-transgenic Mice Markedly Increased Hippmentioning

confidence: 99%

Aberrant adenosine A2A receptor signaling contributes to neurodegeneration and cognitive impairments in a mouse model of synucleinopathy

Ren

Liu

et al. 2016

Experimental Neurology

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Section: Syn Fibrils Into Non-transgenic Mice Markedly Increased Hippmentioning

confidence: 99%

Aberrant adenosine A2A receptor signaling contributes to neurodegeneration and cognitive impairments in a mouse model of synucleinopathy

Ren

Liu

et al. 2016

Experimental Neurology

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“…miRNAs have also been suggested to play an important role in PD and profiled in brains of PD patients (Kim et al, 2007; Minones-Moyano et al, 2011). Among the miRNAs known to be associated with PD, in particular those with postmortem evidence and/or regulating α-synuclein expression, are: miR-34b and miR-34c, down-regulated in the brains of PD patients (Minones-Moyano et al, 2011; Villar-Menendez et al, 2014) and repressing α-synuclein expression (Kabaria et al, 2015); miR-7 and miR-153, suppressing α-synuclein expression (Junn et al, 2009; Doxakis, 2010); miR-433, regulating fibroblast growth factor 20 (FGF20) levels and subsequent α-synuclein expression (Wang et al, 2008); and miR-133b, down-regulated in midbrain of PD patients and interacting with Pitx3 (Kim et al, 2007). In this study, we focused on these six miRNAs to better understand PD-associated changes and explore their potentiality as PD biomarkers.…”

Section: Introductionmentioning

confidence: 99%

Reduced Circulating Levels of miR-433 and miR-133b Are Potential Biomarkers for Parkinson’s Disease

Zhang

Yang

et al. 2017

Front. Cell. Neurosci.

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Aberrant expression of microRNA (miRNA) in tissues may lead to altered level in circulation. Considerable evidence has suggested that miRNA deregulation is involved in the pathogenesis of Parkinson’s disease (PD). In this study, we screened a set of PD-associated miRNAs and aimed to identify differentially expressed miRNAs in plasma of PD patients and to evaluate their potentiality to serve as PD biomarkers. A total of 95 subjects consisting of 46 sporadic PD cases and 49 controls were recruited. Plasma levels of six miRNAs including miR-433, miR-133b, miR-34b, miR-34c, miR-153, and miR-7 were evaluated using reverse transcribed quantitative PCR, among which we found that miR-34c and miR-7 were below detection limit under our condition. The results showed that levels of circulating miR-433 (P = 0.003) and miR-133b (P = 0.006), but not miR-34b and miR-153, were reduced in PD patients. miR-433 and miR-133b were strongly correlated in both control and PD groups (rs = 0.87 and 0.85, respectively). The correlation between miR-34b and miR-153 expressions was significantly reduced (P < 0.05) in the PD group. Although miR-433 and miR-133b were likely to be functionally complimentary as suggested by Pathway and Gene Ontology analyses, these two miRNAs per se might not be sufficient to predict PD. No correlation was observed between the four miRNAs and age or severity of disease. Collectively, our results demonstrate that circulating miR-433 and miR-133b are significantly altered in PD and may serve as PD biomarkers.

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“…The role of miR-34b and miR-34c in the regulation of SNCA transcript levels was also investigated. In human brains, miR-34b and miR-34c are downregulated in PD[9, 10]. The effect of these miRNAs has been investigated in SH-SY5Y cells.…”

Section: Introductionmentioning

confidence: 99%

Genetic analysis of α‐synuclein 3′ untranslated region and its corresponding microRNAs in relation to Parkinson's disease compared to dementia with Lewy bodies

Tagliafierro

Glenn

Zamora

et al. 2017

Alzheimer's & Dementia

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INTRODUCTION The alpha-synuclein (SNCA) gene has been implicated in the etiology of Parkinson’s disease (PD) and Dementia with Lewy Bodies (DLB). METHODS A computational analysis of SNCA-3’UTR to identify potential microRNA binding-sites, and quantitative real-time-PCR to determine their expression in isogenic iPSC-derived dopaminergic and cholinergic neurons as a model of PD and DLB, respectively. Additionally, deep sequencing analysis of SNCA-3’UTR of autopsy confirmed cases of PD, DLB, and normal followed by genetic association analysis of the identified variants. RESULTS We identified four miRNA binding-sites, and observed a neuronal-type specific expression profile for each miRNA in the different isogenic iPSC-derived neurons, i.e. dopaminergic and cholinergic. Furthermore, we found that the short-structural variant rs777296100-polyT was moderately associated with DLB but not with PD. DISCUSSION We suggest that the regulation of SNCA expression through miRNAs is neuronal-type specific, and possibly plays a part in the phenotypic heterogeneity of synucleinopathies. Furthermore, genetic variability in the SNCA gene may contribute to synucleinopathies in a pathology-specific manner.

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Increased striatal adenosine A2A receptor levels is an early event in Parkinson’s disease-related pathology and it is potentially regulated by miR-34b

Cited by 92 publications

References 48 publications

Aberrant adenosine A2A receptor signaling contributes to neurodegeneration and cognitive impairments in a mouse model of synucleinopathy

Aberrant adenosine A2A receptor signaling contributes to neurodegeneration and cognitive impairments in a mouse model of synucleinopathy

Reduced Circulating Levels of miR-433 and miR-133b Are Potential Biomarkers for Parkinson’s Disease

Genetic analysis of α‐synuclein 3′ untranslated region and its corresponding microRNAs in relation to Parkinson's disease compared to dementia with Lewy bodies

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