<i>MicroRNA-195</i>Protects Against Dementia Induced by Chronic Brain Hypoperfusion via Its Anti-Amyloidogenic Effect in Rats

Ai, Jing; Sun, Lihua; Che, Hui; Zhang, Rong; Zhang, Tianzhu; Wu, Wan-Chen; Su, Xiaolin; Chen, Xin; Yang, Guang; Li, Kang; Wang, Ning; Ban, Takahiko; Bao, Yongping; Guo, Fei; Niu, Huifang; Zhu, Yuan Xiao; Zhu, Xiongwei; Yang, Baofeng

doi:10.1523/jneurosci.1997-12.2013

Cited by 103 publications

(168 citation statements)

References 53 publications

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“…Virus-mediated inhibition of miR-195 in the hippocampus resulted in impaired spatial memory in rats as assessed in the Morris water maze [68]. Overexpression of miR-195 in the hippocampus by itself has no enhancing effect on memory formation, but alleviates memory impairments induced by pathological conditions [68].…”

Section: (I) Mir-132mentioning

confidence: 99%

MicroRNAs and synaptic plasticity—a mutual relationship

Aksoy‐Aksel

Zampa

Schratt

2014

Phil. Trans. R. Soc. B

107

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MicroRNAs (miRNAs) are rapidly emerging as central regulators of gene expression in the postnatal mammalian brain. Initial studies mostly focused on the function of specific miRNAs during the development of neuronal connectivity in culture, using classical gain-and loss-of-function approaches. More recently, first examples have documented important roles of miRNAs in plastic processes in intact neural circuits in the rodent brain related to higher cognitive abilities and neuropsychiatric disease. At the same time, evidence is accumulating that miRNA function itself is subjected to sophisticated control mechanisms engaged by the activity of neural circuits. In this review, we attempt to pay tribute to this mutual relationship between miRNAs and synaptic plasticity. In particular, in the first part, we summarize how neuronal activity influences each step in the lifetime of miRNAs, including the regulation of transcription, maturation, gene regulatory function and turnover in mammals. In the second part, we discuss recent examples of miRNA function in synaptic plasticity in rodent models and their implications for higher cognitive function and neurological disorders, with a special emphasis on epilepsy as a disorder of abnormal nerve cell activity.

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Section: (I) Mir-132mentioning

confidence: 99%

MicroRNAs and synaptic plasticity—a mutual relationship

Aksoy‐Aksel

Zampa

Schratt

2014

Phil. Trans. R. Soc. B

107

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“…Therefore, miR-195 and miR-497 are potential therapeutic targets in many types of cancers (Furuta et al, 2013;Guo et al, 2012;Itesako et al, 2014;Li et al, 2011;Ozata et al, 2011). Additionally, miR-195 has been implicated in neurodevelopment (Ai et al, 2013;Liu et al, 2013;Zhu et al, 2012), placental pathogenesis (Bai et al, 2012;Hu et al, 2009) and glucose metabolism (Joglekar et al, 2007;Ortega et al, 2014), suggesting its importance in a range of biological processes.…”

Section: Introductionmentioning

confidence: 99%

The NF-κB-modulated microRNAs miR-195 and miR-497 inhibit myoblast proliferation by targeting Igf1r, Insr and cyclin genes

Wei

Zhang

Bai

et al. 2016

Journal of Cell Science

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MicroRNAs (miRNAs) play important roles in the development of skeletal muscle. In our previous study, expression of miR-195 and miR-497 were shown to be upregulated during muscle development in pigs. In this study, we investigated the roles of these two miRNAs in myogenesis and analyzed their transcriptional regulation. Our results showed that miR-195 and miR-497 were upregulated during muscle development and myoblast differentiation. Moreover, miR-195 and miR-497 inhibited proliferation but not differentiation in C2C12 cells. Further investigation revealed that Igf1r, Insr, Ccnd2 and Ccne1 were directly targeted by miR-195 and miR-497 in myoblasts. In addition, we confirmed that miR-195 and miR-497, which shared the similar expression profiling, were negatively regulated by nuclear factor κB (NF-κB) in both myoblasts and skeletal muscle tissue. Our data illustrate that the signaling pathway NF-κB-miR-195/497-Igf1r/InsrCcnd2/Ccne1 plays important roles in myogenesis. Our study provides novel evidence for the roles of miR-195 and miR-497 in muscle development.

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“…Changes in miR-15a and miR-16 levels have been shown to affect Tau phosphorylation in primary cortical neurons [28]. Moreover, miR-16 directly targets APP [30], and miR-195 has been shown to regulate APP and BACE1 levels, as well as Aβ production [31,32].…”

Section: Introductionmentioning

confidence: 99%

The miR-15/107 Family of microRNA Genes Regulates CDK5R1/p35 with Implications for Alzheimer’s Disease Pathogenesis

et al. 2016

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Cyclin-dependent kinase 5 regulatory subunit 1 (CDK5R1) encodes p35, the main activatory subunit of cyclin-dependent kinase 5 (CDK5). The p35/CDK5 active complex plays a fundamental role in brain development and functioning, but its deregulated activity has also been implicated in various neurodegenerative disorders, including Alzheimer's disease (AD). CDK5R1 displays a large and highly evolutionarily conserved 3′-untranslated region (3′-UTR), a fact that has suggested a role for this region in the post-transcriptional control of CDK5R1 expression. Our group has recently demonstrated that two miRNAs, miR-103 and miR-107, regulate CDK5R1 expression and affect the levels of p35. MiR-103 and miR-107 belong to the miR-15/ 107 family, a group of evolutionarily conserved miRNAs highly expressed in human cerebral cortex. In this work, we tested the hypothesis that other members of this group of miRNAs, in addition to miR-103 and miR-107, were able to modulate CDK5R1 expression. We provide evidence that several miRNAs belonging to the miR-15/107 family regulate p35 levels. BACE1 expression levels were also found to be modulated by different members of this family. Furthermore, overexpression of these miRNAs led to reduced APP phosphorylation levels at the CDK5-specific Thr668 residue. We also show that miR-15/107 miRNAs display reduced expression levels in hippocampus and temporal cortex, but not in cerebellum, of AD brains. Moreover, increased CDK5R1 mRNA levels were observed in AD hippocampus tissues. Our results suggest that the downregulation of the miR-15/ 107 family might have a role in the pathogenesis of AD by increasing the levels of CDK5R1/p35 and consequently enhancing CDK5 activity.

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MicroRNA-195Protects Against Dementia Induced by Chronic Brain Hypoperfusion via Its Anti-Amyloidogenic Effect in Rats

Cited by 103 publications

References 53 publications

MicroRNAs and synaptic plasticity—a mutual relationship

MicroRNAs and synaptic plasticity—a mutual relationship

The NF-κB-modulated microRNAs miR-195 and miR-497 inhibit myoblast proliferation by targeting Igf1r, Insr and cyclin genes

The miR-15/107 Family of microRNA Genes Regulates CDK5R1/p35 with Implications for Alzheimer’s Disease Pathogenesis

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