MiR-214-3p attenuates cognition defects via the inhibition of autophagy in SAMP8 mouse model of sporadic Alzheimer's disease

Zhang, Yueqi; Li, Qiliang; Liu, Chengeng; Gao, Shichao; Pan, Hong; Wang, Jinling; Wang, Peichang

doi:10.1016/j.neuro.2016.07.004

Cited by 66 publications

(46 citation statements)

References 31 publications

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“…It has been reported that miR-214-3p suppresses autophagy by negatively regulating the ATG12 expression. 29 In agreement with this finding, the expression of ATG12 was downregulated by miR-214-3p in the present study, but the repressive effect of miR-214-3p on ATG12 was inhibited by co-transfection with AMO-214-3p, but was not affected by miR-NC or AMO-NC ( Figure 6B). These results were supported by immunofluorescence staining (Figure 6C).…”

Section: Melatonin Ameliorates Neuronal Pyroptosis By Modulating Thsupporting

confidence: 92%

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Che

Yang

et al. 2020

FASEB j.

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Diabetes mellitus (DM) patients are at a higher risk of developing brain injury characterized by neuronal death. Melatonin, a hormone produced by the pineal gland, exerts neuroprotective effects against brain damage. However, the effect of melatonin on diabetes‐induced brain injury has not been elucidated. This study was to evaluate the role of melatonin against neuronal death in DM and to elucidate the underlying mechanisms. Herein, we found that melatonin administration significantly alleviated the neuronal death in both streptozotocin (STZ)‐induced diabetic mice and high glucose (HG)‐treated neuronal cells. Melatonin inhibited neuronal pyroptosis and excessive autophagy, as evidenced by decreased levels of NLRP3, cleaved caspase‐1, GSDMD‐N, IL‐1β, LC3, Beclin1, and ATG12 both in vivo and in vitro. MicroRNA‐214‐3p (miR‐214‐3p) was decreased in DM mice and HG‐treated cells, and such a downregulation was corrected by melatonin, which was accompanied by repression of caspase‐1 and ATG12. Furthermore, downregulation of miR‐214‐3p abrogated the anti‐pyroptotic and anti‐autophagic actions of melatonin in vitro. Our results indicate that melatonin exhibits a neuroprotective effect by inhibiting neuronal pyroptosis and excessive autophagy through modulating the miR‐214‐3p/caspase‐1 and miR‐214‐3p/ATG12 axes, respectively, and it might be a potential agent for the treatment of brain damage in the setting of DM.

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Section: Melatonin Ameliorates Neuronal Pyroptosis By Modulating Thsupporting

confidence: 92%

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Che

Yang

et al. 2020

FASEB j.

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“…Prevention of AD has been reported to be associated with reduction of cognitive impairment (Bennett et al, ). Usually, miRs have been reported to be in association with cognitive function in AD, for instance, miR‐214‐3p has been revealed to relieve cognitive damage in the SAMP8 mouse model of sporadic AD (Zhang et al, ). Interestingly enough, miR‐326 selectively reduced the expression of a neuropeptide urocortin 1 that mediated the brain's stress response (Zhang et al, ).…”

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 addition, stress can induce the interaction between mast cells and microglia and lead to inflammation [58], and inflammation of the [59]. miR-214-3p plays an important role in depressive-like behaviours, cognition defects, Alzheimer's disease, and endothelial cell dysfunction and mediates neural apoptosis, neuropathic pain, and the growth, migration, and invasion of glioma cells [60][61][62][63][64][65]. miR-7-5p is relevant to vascular endothelial cell proliferation, glioma, brain damage, and cognitive dysfunction [66][67][68][69].…”

Section: Journal Of Immunology Researchmentioning

confidence: 99%

Plasma MicroRNA Expression Profiles in Psoriasis

Xiao

Liu

Wang

et al. 2020

Journal of Immunology Research

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Background. Psoriasis is an immune-mediated inflammatory chronic skin disease characterized by chronic inflammation in the dermis, parakeratosis, and excessive epidermal growth. MicroRNAs (miRNAs) are key regulators of immune responses. Although differential expression of miRNAs has been reported in certain inflammatory autoimmune diseases, their role in psoriasis has not been fully illuminated. Our aims were to confirm plasma miRNA expression signatures in psoriasis and to examine their potential influence on psoriasis pathogenesis. Methods. A miRNome PCR array was used to analyse the plasma of psoriasis patients and healthy donors. We performed miRNA pathway enrichment and target gene network analyses on psoriasis plasma samples. Results. We found several specific plasma miRNA signatures relevant to psoriasis. The miRNAs targeted pathways associated with psoriasis, such as the VEGF, MAPK, and WNT signaling pathways. Network analysis revealed pivotal deregulated plasma miRNAs and their relevant target genes and pathways regulating psoriasis pathogenesis. Conclusions. This study analysed the expression of plasma miRNAs and their target pathways, elucidating the pathogenesis of psoriasis; these results may be used to design novel therapeutic strategies and to identify diagnostic biomarkers for psoriasis.

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MiR-214-3p attenuates cognition defects via the inhibition of autophagy in SAMP8 mouse model of sporadic Alzheimer's disease

Cited by 66 publications

References 31 publications

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

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

Plasma MicroRNA Expression Profiles in Psoriasis

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