The Protective Role of microRNA-200c in Alzheimer's Disease Pathologies Is Induced by Beta Amyloid-Triggered Endoplasmic Reticulum Stress

Wu, Qi; Ye, Xiaoyang; Xiong, Yi; Zhu, Haili; Miao, Jianting; Zhang, Wei; Wan, Jun

doi:10.3389/fnmol.2016.00140

Cited by 45 publications

(28 citation statements)

References 33 publications

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“…Considerable evidence demonstrates that the occurrence of AD mutations is closely related to ER stress. PERK and eIF-2α are positively correlated with Aβ plaque aggregation in the brains of AD patients and APP/PS1 mice [14, 39-41]. Molecular alteration in translational machinery through phosphorylation of eIF-2α may play a key role in the pathogenesis of neurodegenerative diseases [40, 42].…”

Section: Discussionmentioning

confidence: 99%

Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Alzheimer disease (AD) is a common neurodegenerative disease that is characterized by the deposition of beta-amyloid peptide and formation of intracellular neurofibrillary tangles. Due to the failure of various clinical trials of novel drugs for AD, effective drugs for AD treatment are urgently required. Methods: In this study, we used the classic APP/PS1 mouse model to explore the neuroprotective effects of a new compound, bajijiasu, and the mechanisms involved. Behavioral tests and western blotting were performed to assess the beneficial effects of bajijiasu in APP/PS1 mice. Results: Morris water maze and Y-maze test results showed that oral administration of bajijiasu (35 mg/kg/day and 70 mg/kg/day) improved learning and memory abilities in APP/PS1 mice. Bajijiasu reduced ROS and MDA levels in both the hippocampus and cortex. Moreover, western blotting results showed that bajijiasu protected neurons from apoptosis, elevated the expression levels of neurotrophic factors, and alleviated endoplasmic reticulum stress in both the hippocampus and cortex. Conclusion: These results indicate that the mechanisms underlying the effects of bajijiasu on AD might be related to beta-amyloid-downstream pathologies, particularly endoplasmic reticulum stress.

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Section: Discussionmentioning

confidence: 99%

Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model

Zhang

et al. 2018

Cell Physiol Biochem

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“…PC12 cells, Neuro2A cells, and HEK293T cells were cultured as described before (Fan et al, 2016; Wu et al, 2016). Primary hippocampal neurons were prepared from embryonic day 18.5 embryos of C57B6 mice.…”

Section: Methodsmentioning

confidence: 99%

“…RNA quantity was measured by NanoDrop 2000 (Thermo Fisher Scientific). cDNA was synthesized, and quantitative PCR (qPCR) was performed as described before (Wu et al, 2016). cDNA was synthesized from 100 ng of total RNA by miR-specific RT primers using a Reverse Transcription System (Promega).…”

Section: Methodsmentioning

confidence: 99%

“…Cells were lysed in RIPA buffer with protease inhibitor cocktail (Thermo Scientific) on ice for half an hour. Brain lysate was harvested and subjected to SDS-PAGE as described before (Wu et al, 2016). Gel-separated proteins were then transferred to NC membrane followed by Western blotting with a primary antibody 1:200 at 4°C overnight and a horseradish peroxidase-conjugated secondary antibody 1:5,000 for 2 h at room temperature.…”

Section: Methodsmentioning

confidence: 99%

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MiR-409-5p as a Regulator of Neurite Growth Is Down Regulated in APP/PS1 Murine Model of Alzheimer’s Disease

Guo

Cai

et al. 2019

Front. Neurosci.

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Alzheimer’s disease (AD) is a heterogeneous neurodegenerative disease. Recent studies suggest that miRNA expression changes are associated with the development of AD. Our previous study showed that the expression level of miR-409-5p was stably downregulated in the early stage of APP/PS1 double transgenic mice model of AD. We now report that miR-409-5p impairs neurite outgrowth, decreases neuronal viability, and accelerates the progression of Aβ1–42-induced pathologies. In this study, we found that Aβ1–42 peptide significantly decreased the expression of miR-409-5p, which was consistent with the expression profile of miR-409-5p in the APP/PS1 mice cortexes. Plek was confirmed to be a potential regulatory target of miR-409-5p by luciferase assay and Western blotting. Overexpression of miR-409-5p has an obvious neurotoxicity in neuronal cell viability and differentiation, whereas Plek overexpression could partially rescue neurite outgrowth from this toxicity. Some cytoskeleton regulatory proteins have been found to be related to AD pathogenesis. Our data show some clues that cytoskeletal reorganization may play roles in AD pathology. The early downregulation of miR-409-5p in AD progression might be a self-protective reaction to alleviate the synaptic damage induced by Aβ, which may be used as a potential early biomarker of AD.

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“…1). The expression levels of miRNAs including miR-135a [13], miR-384 [13], miR-455-3p [14], miR-4668-5p [14], miR-146a-5p, miR-106b-3p, miR-195-5p, miR-20b-5p, and miR-497-5p [15], hsa-miR-101, hsa-miR-155, has-miR-9 [16], miR-206 [17], miR-146a-5p, miR-106b-3p, miR-195-5p, miR-20b-5p, miR-497-5p [15], miR-519 [18], miR-200c [19], miR-590-5p and miR-142-5p [20] were up-regulated, while miR-193b [13], has-miR-501-3p [21], miR-125b-3p, miR-29c-3p, miR-93-5p, miR-19b-3p [15], hsa-let-7d-5p, hsa-let-7g-5p, hsa-miR-15b, has-miR-191-5p, has-miR-26b-5p, hsa-miR-29b, hsa-miR-342-3p [16], miR-135b [22], miR-29, miR-125b [16, 20], miR-223 [18], miR-545-3p [23] and miR-194-5p [20] were down-regulated in serum of AD patients compared with that of normal subjects. In addition, serum miR-206 was enhanced in the individuals with amnestic mild cognitive impairment tend to progress to AD [17].…”

Section: Circulating Mirna and Admentioning

confidence: 99%

The Potential Markers of Circulating microRNAs and long non-coding RNAs in Alzheimer's Disease

Zhao¹,

Zhang²,

Zhang³

et al. 2019

Aging and disease

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Alzheimer’s disease (AD) is a neurodegenerative disorder and one of the leading causes of disability and mortality in the late life with no curative treatment currently. Thus, it is urgently to establish sensitive and non-invasive biomarkers for AD diagnosis, particularly in the early stage. Recently, emerging number of microRNAs (miRNAs) and long-noncoding RNAs (lncRNAs) are considered as effective biomarkers in various diseases as they possess characteristics of stable, resistant to RNAase digestion and many extreme conditions in circulatory fluid. This review highlights recent advances in the identification of the aberrantly expressed miRNAs and lncRNAs in circulatory network for detection of AD. We summarized the abnormal expressed miRNAs in blood and cerebrospinal fluid (CSF), and detailed discussed the functions and molecular mechanism of serum or plasma miRNAs-miR-195, miR-155, miR-34a, miR-9, miR-206, miR-125b and miR-29 in the regulation of AD progression. In addition, we also elaborated the role of circulating lncRNA major including beta-site APP cleaving enzyme 1 (BACE1) and its antisense lncRNA BACE1-AS in AD pathological advancement. In brief, confirming the aberrantly expressed circulating miRNAs and lncRNAs will provide an effective testing tools for treatment of AD in the future.

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The Protective Role of microRNA-200c in Alzheimer's Disease Pathologies Is Induced by Beta Amyloid-Triggered Endoplasmic Reticulum Stress

Cited by 45 publications

References 33 publications

Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model

Bajijiasu Ameliorates β-Amyloid-Triggered Endoplasmic Reticulum Stress and Related Pathologies in an Alzheimer’s Disease Model

MiR-409-5p as a Regulator of Neurite Growth Is Down Regulated in APP/PS1 Murine Model of Alzheimer’s Disease

The Potential Markers of Circulating microRNAs and long non-coding RNAs in Alzheimer's Disease

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