Trasferrin receptor 2 gene regulation by microRNA 221 in SH-SY5Y cells treated with MPP+ as Parkinson's disease cellular model

Asci, Roberta; Vallefuoco, Fara; Andolfo, Immacolata; Bruno, Mariasole; Falco, Luigia De; Iolascon, Achille

doi:10.1016/j.neures.2013.09.003

Cited by 24 publications

(13 citation statements)

References 31 publications

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“…According to neurology, miR‐221 was highly expressed in the glioma cells and suppression of miR‐221 resulted in decreased cellular proliferation, migration, and invasion . Furthermore, miR‐221 was reported to regulate transferrin receptor type 2 in PD model, related to iron accumulation, which directly contributes to neurodegeneration . These data provide evidence of the expression of circulating miR‐221 in a highly coordinated manner with pathological processes of PD and further indicate that miR‐221 might be involved in regulating cell apoptosis and fibrosis, which are likely involved in the initiation inflammation process of PD neuropathogenesis.…”

Section: Discussionmentioning

confidence: 73%

Serum miR‐221 serves as a biomarker for Parkinson's disease

Wang

et al. 2016

Cell Biochemistry & Function

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Parkinson's disease (PD) is the common age-related neurodegenerative disorder. Sensitive, noninvasive biomarkers that facilitate PD diagnosis and stage assignment are currently unavailable. This study aims to investigate the potential of 16 previous reported PD-associated miRNAs as novel biomarkers for PD. The expression of 16 serum miRNAs was measured by quantitative reverse transcriptase polymerase chain reaction in 138 PD patients and 112 control populations. Analyses were undertaken to assess the specificity and sensitivity of miRNAs to predict PD. In addition, the relationship between deregulated miRNAs and Part III of the United Parkinson's Disease Rating Scale (UPDRS-III) and Part V of the UPDRS (UPDRS-V; the modified Hoehn and Yahr staging of PD) in PD patients was also assessed. It was found that the serums miR-29c, miR-146a, miR-214, and miR-221 were significantly decreased in PD patients compared with healthy control populations. In addition, serum miR-221 was positively correlated with UPDRS-III (r = .4702) and UPDRS-V (r = .4788) score in PD patients. Furthermore, the receiver operating characteristic result of serum miR-221 for prediction of PD was 0.787. Our preliminary findings indicate that downregulated serum miR-221 might be a potential biomarker for PD evaluation.

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Section: Discussionmentioning

confidence: 73%

Serum miR‐221 serves as a biomarker for Parkinson's disease

Wang

et al. 2016

Cell Biochemistry & Function

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“…Previous studies have uncovered the regulation of miRNAs by MPP + in DA neurons or their cell lines (Asci et al, ; Niu, Xu, Wang, Hou, & Xie, ), while little is known about miRNA regulation by MPP + in microglia. Thus, one of the important findings of this study is that miR‐7116‐5p in microglia is downregulated by MPP + .…”

Section: Discussionmentioning

confidence: 99%

Downregulation of miR‐7116‐5p in microglia by MPP⁺ sensitizes TNF‐α production to induce dopaminergic neuron damage

Wang

Yuan³

et al. 2017

Glia

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Activation of microglia resulting in exacerbated inflammation expression plays an important role in degeneration of dopaminergic (DA) neurons in the pathogenesis of Parkinson's disease (PD). However, how this enhanced inflammation is induced in microglia remains largely unclear. Here, in the mouse PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetra hydropyridine (MPTP), we found that miR-7116-5p in microglia has a crucial role in this inflammation. 1-methyl-4-phenylpyridinium (MPP ) is uptaken by microglia through organic cation transporter 3 (OCT3) to downregulate miR-7116-5p, an miRNA found to target tumor necrosis factor alpha (TNF-α). Production of TNF-α in microglia is specifically potentiated by MPP via downregulation of miR-7116-5p to elicit subsequent inflammatory responses. Furthermore, enhancement of miR-7116-5p expression in microglia in mice inhibits the production of TNF-α and the activation of glia, and further prevents loss of DA neurons. Together, our studies suggest that MPP suppresses miR-7116-5p level in microglia and potentiates TNF-α production and inflammatory responses to contribute to DA neuron damage.

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“…F) However, c-Fos mRNA levels were similar between genotypes at 12 months in the ventral hippocampus. G) Representative blots of the data presented in A-B, D-E. * p < 0.05. diseases [44,45]. Fourty-eight hours after transfection of miR-181 or a non-related sequence as a negative control, the steady-state levels of SIRT-1 and c-Fos were determined.…”

Section: Overexpression Of Mir-181 Decreased Protein Levels Of Sirt-1mentioning

confidence: 99%

Upregulation of miR-181 Decreases c-Fos and SIRT-1 in the Hippocampus of 3xTg-AD Mice

Rodriguez‐Ortiz

Baglietto‐Vargas

Martínez-Coria

et al. 2014

JAD

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MicroRNAs are a group of small RNAs that regulate diverse cellular processes including neuronal function. Recent studies have shown that dysregulation of specific microRNAs is critically involved in the development of Alzheimer's disease (AD). Most of these reports have focused on microRNAs implicated in alterations of amyloid-β and tau. However, studies exploring the relation between microRNAs dysregulation in AD and synaptic plasticity are scarce despite the well-known involvement of microRNAs in synaptic plasticity. Since impairments in synaptic plasticity and neuronal loss are two important features displayed in AD patients, it is feasible to hypothesize that alterations in plasticity-related microRNAs underlie AD progression. Here, levels of a small number of microRNAs implicated in normal neuronal function and/or plasticity were examined in an AD model. Twelve-month old 3xTg-AD mice with plaques and tangles presented a significant upregulation of miR-181 in the hippocampus compared to age-matched wild type mice. Increased miR-181 was not detected in pre-pathological 3xTg-AD mice. Analysis of predicted targets of miR-181 identified c-Fos and SIRT-1, proteins critically involved in memory formation. Both c-Fos and SIRT-1 levels were significantly decreased in the ventral hippocampus of twelve-month old 3xTg-AD mice. Overexpression of miR-181 in SH-SY5Y cells significantly decreased c-Fos and SIRT-1, strongly suggesting that miR-181 directly regulates the expression of these two proteins. These findings indicate a connection between miR-181 and proteins involve in synaptic plasticity and memory processing in a transgenic mouse model of AD. Our results suggest that microRNAs involved in synaptic plasticity might be an important factor that contributes to AD neuropathology.

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Trasferrin receptor 2 gene regulation by microRNA 221 in SH-SY5Y cells treated with MPP+ as Parkinson's disease cellular model

Cited by 24 publications

References 31 publications

Serum miR‐221 serves as a biomarker for Parkinson's disease

Serum miR‐221 serves as a biomarker for Parkinson's disease

Downregulation of miR‐7116‐5p in microglia by MPP⁺ sensitizes TNF‐α production to induce dopaminergic neuron damage

Upregulation of miR-181 Decreases c-Fos and SIRT-1 in the Hippocampus of 3xTg-AD Mice

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Trasferrin receptor 2 gene regulation by microRNA 221 in SH-SY5Y cells treated with MPP+ as Parkinson's disease cellular model

Cited by 24 publications

References 31 publications

Serum miR‐221 serves as a biomarker for Parkinson's disease

Serum miR‐221 serves as a biomarker for Parkinson's disease

Downregulation of miR‐7116‐5p in microglia by MPP+ sensitizes TNF‐α production to induce dopaminergic neuron damage

Upregulation of miR-181 Decreases c-Fos and SIRT-1 in the Hippocampus of 3xTg-AD Mice

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Downregulation of miR‐7116‐5p in microglia by MPP⁺ sensitizes TNF‐α production to induce dopaminergic neuron damage