MicroRNA-195 downregulates Alzheimer's disease amyloid-β production by targeting BACE1

Zhu, Hang; Wang, Limei; Wang, Miao; Song, Bo; Tan, Song; Teng, Jie; Duan, Dong-Xiao

doi:10.1016/j.brainresbull.2012.05.018

Cited by 170 publications

(88 citation statements)

References 35 publications

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“…mmumiR-195 has previously been reported to target the mRNA of the beta-site APP cleaving enzyme 1 (BACE1) in SAMP8 mice, which down-regulates β-amyloid production by inhibiting expression of BACE1 (Zhu et al 2012). This negative feedback mechanism may also be present in this mouse model, since mice show the presence of amyloid plaques at 20 mo of age.…”

Section: Differentially Expressed Ncrnas In Young Mice Of the 3xtg Momentioning

confidence: 89%

Generation of a neuro-specific microarray reveals novel differentially expressed noncoding RNAs in mouse models for neurodegenerative diseases

Gstir

Schafferer

Scheideler

et al. 2014

RNA

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We have generated a novel, neuro-specific ncRNA microarray, covering 1472 ncRNA species, to investigate their expression in different mouse models for central nervous system diseases. Thereby, we analyzed ncRNA expression in two mouse models with impaired calcium channel activity, implicated in Epilepsy or Parkinson's disease, respectively, as well as in a mouse model mimicking pathophysiological aspects of Alzheimer's disease. We identified well over a hundred differentially expressed ncRNAs, either from known classes of ncRNAs, such as miRNAs or snoRNAs or which represented entirely novel ncRNA species. Several differentially expressed ncRNAs in the calcium channel mouse models were assigned as miRNAs and target genes involved in calcium signaling, thus suggesting feedback regulation of miRNAs by calcium signaling. In the Alzheimer mouse model, we identified two snoRNAs, whose expression was deregulated prior to amyloid plaque formation. Interestingly, the presence of snoRNAs could be detected in cerebral spine fluid samples in humans, thus potentially serving as early diagnostic markers for Alzheimer's disease. In addition to known ncRNAs species, we also identified 63 differentially expressed, entirely novel ncRNA candidates, located in intronic or intergenic regions of the mouse genome, genomic locations, which previously have been shown to harbor the majority of functional ncRNAs.

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Section: Differentially Expressed Ncrnas In Young Mice Of the 3xtg Momentioning

confidence: 89%

Generation of a neuro-specific microarray reveals novel differentially expressed noncoding RNAs in mouse models for neurodegenerative diseases

Gstir

Schafferer

Scheideler

et al. 2014

RNA

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“…Therefore, miR-135b may be a potential candidate for the treatment of AD through inhibiting BACE1. In addition, several other miRs have been observed to directly target BACE1, including the miR-29 family, miR-124, miR-195 and miR-339-5p, and thus may contribute to the treatment of AD (4,(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

Zhang

Xing

Guo

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) are a class of endogenous small non-coding RNAs that have been revealed to negatively mediate the expression of their target genes at the post-transcriptional level. Recently, particular miRs have demonstrated an involvement in the pathogenesis of Alzheimer's disease (AD). However, the specific role of miR-135b in AD has yet to be elucidated. The present study aimed to investigate the neuroprotective role of miR-135b, in addition to its underlying mechanism. Herein, reverse transcription-quantitative polymerase chain reaction was conducted to determine miR-135b expression levels in the peripheral blood samples of patients with AD and age-matched normal controls. The data of the present study revealed that the expression levels of miR-135b were significantly reduced in the peripheral blood of AD patients compared with normal controls (P<0.01). In vitro MTT analyses identified that the overexpression of miR-135b significantly enhanced the proliferation of hippocampal cells (P<0.01). Furthermore, in vivo analysis using a Y-maze test indicated that injection with miR-135b mimics into the third ventricle of anesthetized SAMP8 mice significantly enhanced their learning and memory capacities (P<0.01). Molecular mechanism investigations identified β-site APP-cleaving enzyme 1 (BACE1) as a direct target gene of miR-135b, and the latter was identified to negatively mediate the protein expression levels of BACE1 in hippocampal cells, in addition to hippocampal tissues, of SAMP8 mice. Based on the aforementioned findings, we propose that miR-135b has a neuroprotective role via direct targeting of BACE1 and, thus, may be used for the treatment of AD.

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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-ҡB modulated miR-195/497 inhibit myoblast proliferation by targeting Igf1r/Insr and cyclin genes

Wei

Zhang

Bai

et al. 2015

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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MicroRNA-195 downregulates Alzheimer's disease amyloid-β production by targeting BACE1

Cited by 170 publications

References 35 publications

Generation of a neuro-specific microarray reveals novel differentially expressed noncoding RNAs in mouse models for neurodegenerative diseases

Generation of a neuro-specific microarray reveals novel differentially expressed noncoding RNAs in mouse models for neurodegenerative diseases

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

The NF-ҡB modulated miR-195/497 inhibit myoblast proliferation by targeting Igf1r/Insr and cyclin genes

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