Adenosine A2A Receptor Expression in Peripheral Blood Mononuclear Cells of Patients with Mild Cognitive Impairment

Arosio, Beatrice; Viazzoli, Chiara; Mastronardi, L.; Bilotta, Claudio; Vergani, Carlo; Bergamaschini, Luigi

doi:10.3233/jad-2010-090814

Cited by 20 publications

(16 citation statements)

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“…Moreover, it can be appreciated from the scatter dot plots that although the two distributions of activity data are very much alike with comparable median values, in the case of the LOAD group a greater number of subjects fall below the median value. These observations support the notion that Ser 16 phosphorylation may not be the only mechanism involved in the modulation of Pin1 activity [26] .…”

Section: Discussionsupporting

confidence: 79%

“…There can be different interpretations to this finding: (a) the presence in LOAD patients of rare gene variants of Pin1 that could influence its phosphorylation state [24] ; (b) the effects on Pin1 of a higher blood concentration of A ␤ 1-42 [25] ; indeed, in rat hippocampal cells, treatment with A ␤ 1-42 oligomers has been shown to promote a transient Pin1 dephosphorylation on Ser 16 associated with a decrease in phosphorylated TauThr231 [9] ; and (c) a LOAD-associated dysregulation in the kinases and phosphatases that control Pin1 phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

“…Data were normalized to the endogenous reference gene glyceraldehyde-3-phosphate dehydrogenase. The relative quantification of Pin1 mRNA expression was carried out as previously described [16,17] .…”

Section: Pin1 Gene Expression and Promoter Methylationmentioning

confidence: 99%

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Pin1 Contribution to Alzheimer’s Disease: Transcriptional and Epigenetic Mechanisms in Patients with Late-Onset Alzheimer’s Disease

Arosio¹,

Bulbarelli²,

Candia³

et al. 2012

Neurodegener Dis

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Background: Neurofibrillary tangles and senile plaques are hallmarks of Alzheimer’s disease (AD) although the molecular basis of their coexistence remains elusive. The peptidyl-prolyl cis/trans isomerase Pin1 acts on both tau and amyloid precursor protein to regulate their functions by influencing tau phosphorylation and amyloid precursor protein processing. Objective: In order to identify potential biomarkers for AD in easily accessible cells and to gain insight into the relationship between the brain and peripheral compartments in AD pathology, we investigated Pin1 expression and activity in the peripheral blood mononuclear cells of subjects with late-onset AD (LOAD) and age-matched controls (CT). Methods: Gene and protein expression, promoter methylation, Ser¹⁶ phosphorylation and activity of Pin1 were evaluated in 32 samples from subjects with LOAD and in 28 samples from CT. Results: In LOAD subjects, there was a statistically significant reduction in Ser¹⁶ phosphorylation (–30%; p = 0.041) and promoter methylation (–8%; p = 0.001), whereas Pin1 expression was significantly increased (+74%; p = 0.018). Conclusion: The modifications of Pin1 found in LOAD subjects support its involvement in the pathogenesis of the disease with an important role being played by epigenetic mechanisms.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

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Pin1 Contribution to Alzheimer’s Disease: Transcriptional and Epigenetic Mechanisms in Patients with Late-Onset Alzheimer’s Disease

Arosio¹,

Bulbarelli²,

Candia³

et al. 2012

Neurodegener Dis

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“…Genomic DNA was extracted by the salting-out method as described previously (Arosio et al, 2010). First, DNA underwent bisulfite modification to convert unmethylated cytosine residues to uracil, using the CpGenome DNA Modification Kit (Chemicon International, Purchase, NY), according to the manufacturer's instructions.…”

Section: Bdnf Gene Promoter Methylationmentioning

confidence: 99%

Selective DNA Methylation of BDNF Promoter in Bipolar Disorder: Differences Among Patients with BDI and BDII

D’Addario

Dell’Osso

Palazzo

et al. 2012

Neuropsychopharmacol

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164

109

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The etiology of bipolar disorder (BD) is still poorly understood, involving genetic and epigenetic mechanisms as well as environmental contributions. This study aimed to investigate the degree of DNA methylation at the promoter region of the brain-derived neurotrophic factor (BDNF) gene, as one of the candidate genes associated with major psychoses, in peripheral blood mononuclear cells isolated from 94 patients with BD (BD I ¼ 49, BD II ¼ 45) and 52 healthy controls. A significant BDNF gene expression downregulation was observed in BD II 0.53±0.11%; Po0.05), but not in BD I (1.13±0.19%) patients compared with controls (CONT: 1±0.2%). Consistently, an hypermethylation of the BDNF promoter region was specifically found in BD II patients (CONT: 24.0±2.1%; BDI: 20.4±1.7%; BDII: 33.3 ± 3.5%, Po0.05). Of note, higher levels of DNA methylation were observed in BD subjects on pharmacological treatment with mood stabilizers plus antidepressants (34.6 ± 4.2%, predominantly BD II) compared with those exclusively on mood-stabilizing agents (21.7 ± 1.8%; Po0.01, predominantly BD I). Moreover, among the different pharmacological therapies, lithium (20.1 ± 3.8%, Po0.05) and valproate (23.6 ± 2.9%, Po0.05) were associated with a significant reduction of DNA methylation compared with other drugs (35.6 ± 4.6%). Present findings suggest selective changes in DNA methylation of BDNF promoter in subjects with BD type II and highlight the importance of epigenetic factors in mediating the onset and/or susceptibility to BD, providing new insight into the mechanisms of gene expression. Moreover, they shed light on possible mechanisms of action of mood-stabilizing compounds vs antidepressants in the treatment of BD, pointing out that BDNF regulation might be a key target for their effects.

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“…This work defined two subgroups of centenarians with high and low values of basic immune parameters [23]. On the other hand, the group of Bergamaschini detected different levels of ADORA2A mRNA and its cognate receptor in patients with diverse grade of cognitive impairment [24]. Our statistical analysis on mental damage in both centenarian subgroups indicates, that their grade of cognitive impairment, is independent of ADORA2A mRNA levels.…”

Section: Discussionmentioning

confidence: 95%

Low expression of CD39 and CD73 genes in centenarians compared with octogenarians

et al. 2017

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Ageing involves a progressive decline of the body’s regulatory systems including immune system. Adenosine regulates immune function by interaction with its receptors, mainly adenosine A2A receptor, present on the surface of immune cells. Furthermore, cellular response to this nucleoside is highly dependent on its extracellular concentration that is regulated by ecto-enzymes such as CD39 and CD73. Therefore, the aim of this study was to investigate the effect of age on adenosine A2A receptor, CD39 and CD73 gene expression. Changes in mRNA were measured by quantitative PCR from peripheral blood of young, middle-aged and older adults as well as centenarians. Centenarians showed a prominent decrease of CD39 and CD73 mRNA in comparison with older adults. Regarding to adenosine A2A receptor, we detected two subgroups of centenarians with high and low level of transcript. Additionally, adenosine A2A receptor mRNA level of centenarians, did not correlate with their cognitive impairment. In summary, our pilot study suggests that unlike of adenosine A2A receptor, the level of CD39 as well as CD73 mRNA could be a hallmark of successful human ageing.Electronic supplementary materialThe online version of this article (doi:10.1186/s12979-017-0094-3) contains supplementary material, which is available to authorized users.

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Adenosine A2A Receptor Expression in Peripheral Blood Mononuclear Cells of Patients with Mild Cognitive Impairment

Cited by 20 publications

References 0 publications

Pin1 Contribution to Alzheimer’s Disease: Transcriptional and Epigenetic Mechanisms in Patients with Late-Onset Alzheimer’s Disease

Pin1 Contribution to Alzheimer’s Disease: Transcriptional and Epigenetic Mechanisms in Patients with Late-Onset Alzheimer’s Disease

Selective DNA Methylation of BDNF Promoter in Bipolar Disorder: Differences Among Patients with BDI and BDII

Low expression of CD39 and CD73 genes in centenarians compared with octogenarians

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