<i>Retracted</i>: Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

Zhou, Ying; Wang, Zhoufan; Li, Wei; Hong, Hui; Chen, Juan; Tian, Yange; Liu, Zhaoyun

doi:10.1002/jcb.26700

Cited by 53 publications

(32 citation statements)

References 45 publications

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“…Furthermore, circulating miR‐7 levels have been shown to increase in schizophrenia patients . The disease duration was positively correlated with miR‐330‐5p, an miRNA that has been predicted to regulate activity‐dependent mRNAs in the hippocampus and protect neurons from amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease . Last, we found no significant correlation between miRNA relative expression and sex, indicating that neuronal miRNA levels are not the primary driver of sex‐linked differences in PD.…”

Section: Discussionmentioning

confidence: 60%

Circulating Brain‐Enriched MicroRNAs for Detection and Discrimination of Idiopathic and Genetic Parkinson's Disease

et al. 2019

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Background A minimally invasive test for early detection and monitoring of Parkinson's disease (PD) is a highly unmet need for drug development and planning of patient care. Blood plasma represents an attractive source of biomarkers. MicroRNAs (miRNAs) are conserved noncoding RNA molecules that serve as posttranscriptional regulators of gene expression. As opposed to ubiquitously expressed miRNAs that control house‐keeping processes, brain‐enriched miRNAs regulate diverse aspects of neuron development and function. These include neuron‐subtype specification, axonal growth, dendritic morphogenesis, and spine density. Backed by a large number of studies, we now know that the differential expression of neuron‐enriched miRNAs leads to brain dysfunction. Objectives The aim was to identify subsets of brain‐enriched miRNAs with diagnostic potential for familial and idiopathic PD as well as specify the molecular pathways deregulated in PD. Methods Initially, brain‐enriched miRNAs were selected based on literature review and validation studies in human tissues. Subsequently, real‐time reverse transcription polymerase chain reaction was performed in the plasma of 100 healthy controls and 99 idiopathic and 53 genetic (26 alpha‐synucleinA53T and 27 glucocerebrosidase) patients. Statistical and bioinformatics analyses were carried out to pinpoint the diagnostic biomarkers and deregulated pathways, respectively. Results An explicit molecular fingerprint for each of the 3 PD cohorts was generated. Although the idiopathic PD fingerprint was different from that of genetic PD, the molecular pathways deregulated converged between all PD subtypes. Conclusions The study provides a group of brain‐enriched miRNAs that may be used for the detection and differentiation of PD subtypes. It has also identified the molecular pathways deregulated in PD. © 2019 International Parkinson and Movement Disorder Society

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Section: Discussionmentioning

confidence: 60%

Circulating Brain‐Enriched MicroRNAs for Detection and Discrimination of Idiopathic and Genetic Parkinson's Disease

et al. 2019

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“…In addition, VAV1 has been identified as an ineffective stimulus for the JNK1 pathway in T cells (Kaminski, Del Pozo, Hipskind, Altman, & Villalba, ). Besides, miR‐330 protects against β‐protein production and oxidative stress in AD by mediating JNK via targeting VAV1 (Zhou et al, ). Our study has clarified that upregulating miR‐326 subsequently decreased tau phosphorylation by decreasing the expression of VAV1 and inactivating JNK signaling pathway, therefore exerting protective effects against AD.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐326 decreases tau phosphorylation and neuron apoptosis through inhibition of the JNK signaling pathway by targeting VAV1 in Alzheimer's disease

Chen

Zeng

et al. 2019

Journal Cellular Physiology

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Alzheimer's disease (AD) is a progressive and age-related neurological dysfunction.Abundant data have profiled microRNA (miR) patterns in healthy, aging brain, and in the moderate and late-stages of AD. Herein, this study aimed to explore whether miR-326 could influence neuron apoptosis in AD mice and how miR-326 functions in this process. The candidate differentially expressed gene VAV1 was obtained by microarray analysis, and miRNAs that could regulate VAV1 candidate gene were predicted. Luciferase activity determination confirmed VAV1 as a target gene of miR-326. AD mice models were established for investigating the effect of miR-326 on AD mice. The overexpression of miR-326 contributed to decreased time of the mice to find the platform and the escape latency and increased residence time on the target area. Besides, elevation of miR-326 decreased Aβ deposition and contents of Aβ 1-40 and Aβ 1-42 . Moreover, miR-326 overexpression increased neuron cell ability, mediated cell entry, and inhibited neuron apoptosis via JNK signaling pathway. Of crucial importance, miR-326 negatively regulated the expression of VAV1, inhibited tau phosphorylation, and blocked the activation of the JNK signaling pathway. Taken together these observations, we demonstrate that miR-326 improves cognitive function of AD mice and inhibits neuron apoptosis in AD mice through inactivation of the JNK signaling pathway by targeting VAV1. Based on those findings, miR-326 might exert promise as target for the treatment of AD.

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“…In the sight of this, additional studies are necessary to validate the impacts of miR-98 in the regulation of AD mice by targeting HEY2 through the Notch signaling pathway before its consideration as an appropriate treatment for AD. Zhou et al [ 50 ] described the effect of miRNA targeting proto-oncogene vav (VAV) on Aβ production, oxidative stress and mitochondrial malfunction in AD mice through the MAPK signaling pathway.…”

Section: Mirna Dysregulation and Mitochondrial Dysfunction In Alzhmentioning

confidence: 99%

MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases

Catanesi

d’Angelo

Tupone

et al. 2020

IJMS

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Neurodegenerative diseases are debilitating and currently incurable conditions causing severe cognitive and motor impairments, defined by the progressive deterioration of neuronal structure and function, eventually causing neuronal loss. Understand the molecular and cellular mechanisms underlying these disorders are essential to develop therapeutic approaches. MicroRNAs (miRNAs) are short non-coding RNAs implicated in gene expression regulation at the post-transcriptional level. Moreover, miRNAs are crucial for different processes, including cell growth, signal transmission, apoptosis, cancer and aging-related neurodegenerative diseases. Altered miRNAs levels have been associated with the formation of reactive oxygen species (ROS) and mitochondrial dysfunction. Mitochondrial dysfunction and ROS formation occur in many neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s diseases. The crosstalk existing among oxidative stress, mitochondrial dysfunction and miRNAs dysregulation plays a pivotal role in the onset and progression of neurodegenerative diseases. Based on this evidence, in this review, with a focus on miRNAs and their role in mitochondrial dysfunction in aging-related neurodegenerative diseases, with a focus on their potential as diagnostic biomarkers and therapeutic targets.

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Retracted: Protective effects of microRNA‐330 on amyloid β‐protein production, oxidative stress, and mitochondrial dysfunction in Alzheimer's disease by targeting VAV1 via the MAPK signaling pathway

Cited by 53 publications

References 45 publications

Circulating Brain‐Enriched MicroRNAs for Detection and Discrimination of Idiopathic and Genetic Parkinson's Disease

Circulating Brain‐Enriched MicroRNAs for Detection and Discrimination of Idiopathic and Genetic Parkinson's Disease

MicroRNA‐326 decreases tau phosphorylation and neuron apoptosis through inhibition of the JNK signaling pathway by targeting VAV1 in Alzheimer's disease

MicroRNAs Dysregulation and Mitochondrial Dysfunction in Neurodegenerative Diseases

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