MiR-138/SIRT1 axis is implicated in impaired learning and memory abilities of cerebral ischemia/reperfusion injured rats

Tian, Feng; Yuan, Chao; Yue, Hongmei

doi:10.1016/j.yexcr.2018.03.042

Cited by 23 publications

(17 citation statements)

References 34 publications

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“…We also found that there are classical and evolutionarily conserved miR‐138‐5p binding sites in 3′‐UTR region of SIRT1 by TargetScan analysis (Figure A). In addition, study has confirmed the specific targeting by miR‐138‐5p of the SIRT1, which was also supported by our results (Figure B). Therefore, the increasing of SIRT1 expression might be resulted from Mn inhibiting the expression of miRNA‐138‐5p (Figures A and A‐C).…”

Section: Discussionsupporting

confidence: 90%

“…The role of miRNAs is mainly achieved through combination with the base of the 3′‐untranslated region (3′‐UTR) of the target gene mRNAs to suppress their expressions by degradation and translational inhibition . A single miRNA can regulate hundreds of target gene mRNAs, and a single target gene mRNA can be regulated by several different miRNAs, such as microRNA‐138‐5p (miR‐138‐5p), miRNA‐34a, miRNA‐204, and miRNA‐23a all can target and regulate SIRT1 . Evidences suggest that miRNA‐138‐5p is highly expressed in nervous system and exerts an important role in regulating memory and axon regeneration .…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of miR‐138‐5p suppresses MnCl₂‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells

Zhang

et al. 2019

Environmental Toxicology

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The mechanism of manganism caused by manganese (Mn), an important environmental risk factor for Parkinson's disease, is still unclear. Recent evidence suggested that autophagy participated in neurodegenerative diseases, in which microRNA played a crucial role. However, roles of microRNA in the aberrant autophagy that occurs in neurodegenerative diseases remains controversial. In nervous system, miRNA-138-5p is highly expressed and plays a key role in regulating memory and axon regeneration. Importantly, we also found that miR-138-5p expression decreased significantly after SH-SY5Y cells exposed to manganese chloride (MnCl 2 ) in previous study. To explore the role of miR-138-5p in Mn-induced autophagy, autophagy associated indicators were detected. And we found that MnCl 2 could induce autophagic dysregulation and inhibit expression of miR-138-5p. While the levels of LC3-II/LC3-I, Beclin1, and p62, the number of autophagosome formation significantly decreased after miR-138-5p over-expression, which demonstrated that miR-138-5p could clearly retard Mn-induced autophagy. In additional, we found there were classical and evolutionarily conserved miR-138-5p binding sites in 3 0 -UTR region of SIRT1, which was inhibited when overexpression of miR-138-5p. Therefore, it was speculated that elevated expression of SIRT1 may be resulted from inhibition of miR-138-5p after cells exposed to MnCl 2 . Finally, we found that SIRT1 inhibitor EX-527 suppressed Mn-induced autophagy as well as miR-138-5p, while the suppression was reversed by SIRT1-specific activator SRT1720. These results indicated that overexpression of miR-138-5p suppressed Mn-induced autophagy by targeting SIRT1. K E Y W O R D S autophagy, manganese, MicroRNA-138-5p, SIRT1

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Overexpression of miR‐138‐5p suppresses MnCl₂‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells

Zhang

et al. 2019

Environmental Toxicology

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“…In addition, TGFβ mediated suppression of SIRT1 expression leading to the activation of Notch signaling pathway in ECs was reported to be depended partly on miR-212 (153). Further, a key micro regulator of angiogenesis and hypoxia responses, miR-138-P_5P has been reported to target SIRT1 (154)(155)(156).…”

Section: Post Transcriptional Regulation Of Sirtuins: Importance Of Mmentioning

confidence: 99%

Role of Sirtuins in Tumor Angiogenesis

et al. 2020

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Generally, changes in the metabolic status of cells under conditions like hypoxia and accumulation of lactate can be sensed by various sensing mechanisms, leading to modulation of a number of signal transduction pathways and transcription factors. Several of the proangiogenic cytokines like VEGF, FGF, PDGF, TGF-β, Ang-2, ILs, etc. are secreted by cancer cells, under hypoxic microenvironment. These cytokines bind to their receptors on the endothelial cells and activates a number of signaling pathways including Akt/PIP3, Src, p38/MAPK, Smad2/3, etc., which ultimately results in the proliferation and migration of endothelial cells. Transcription factors that are activated in response to the metabolic status of tumors include HIFs, NF-κb, p53, El-2, and FOXO. Many of these transcription factors has been reported to be regulated by a class of histone deacetylase called sirtuins. Sirtuins are NAD + dependent histone deacetylases that play pivotal role in the regulation of tumor cell metabolism, proliferation, migration and angiogenesis. The major function of sirtuins include, deacetylation of histones as well as some non-histone proteins like NF-κB, FOXOs, PPAR , PGC1-α, enzymes like acetyl coenzymeA and structural proteins like α tubulin. In the cell, sirtuins are generally considered as the redox sensors and their activities are dependent on the metabolic status of the cell. Understanding the intricate regulatory mechanisms adopted by sirtuins, is crucial in devising effective therapeutic strategies against angiogenesis, metastasis and tumor progression. Keeping this in mind, the present review focuses on the role of sirtuins in the process of tumor angiogenesis and the regulatory mechanisms employed by them.

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“…The control of miRNAs on gene expression could lead to different functional outcomes. A clear role of miR138-P1_5p in homeostasis and tissue remodeling already has been demonstrated, 81 possibly due to its ability also to control sirtuin genes (i.e., SIRT-1). This miRNA also seems to play a role in angiogenesis and hypoxia response.…”

Section: Main Textmentioning

confidence: 99%

Potential Role of miRNAs as Theranostic Biomarkers of Epilepsy

Cava

Manna

Gambardella

et al. 2018

Molecular Therapy - Nucleic Acids

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Epilepsy includes a group of disorders of the brain characterized by an enduring predisposition to generate epileptic seizures. Although familial epilepsy has a genetic component and heritability, the etiology of the majority of non-familial epilepsies has no known associated genetic mutations. In epilepsy, recent epigenetic profiles have highlighted a possible role of microRNAs in its pathophysiology. In particular, molecular profiling identifies a significant number of microRNAs (miRNAs) altered in epileptic hippocampus of both animal models and human tissues. In this review, analyzing molecular profiles of different animal models of epilepsy, we identified a group of 20 miRNAs commonly altered in different epilepsy-animal models. As emerging evidences highlighted the poor overlap between signatures of animal model tissues and human samples, we focused our analysis on miRNAs, circulating in human biofluids, with a principal role in epilepsy hallmarks, and we identified a group of 8 diagnostic circulating miRNAs. We discussed the functional role of these 8 miRNAs in the epilepsy hallmarks. A few of them have also been proposed as therapeutic molecules for epilepsy treatment, revealing a great potential for miRNAs as theranostic molecules in epilepsy.

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MiR-138/SIRT1 axis is implicated in impaired learning and memory abilities of cerebral ischemia/reperfusion injured rats

Cited by 23 publications

References 34 publications

Overexpression of miR‐138‐5p suppresses MnCl₂‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells

Overexpression of miR‐138‐5p suppresses MnCl₂‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells

Role of Sirtuins in Tumor Angiogenesis

Potential Role of miRNAs as Theranostic Biomarkers of Epilepsy

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MiR-138/SIRT1 axis is implicated in impaired learning and memory abilities of cerebral ischemia/reperfusion injured rats

Cited by 23 publications

References 34 publications

Overexpression of miR‐138‐5p suppresses MnCl2‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells

Overexpression of miR‐138‐5p suppresses MnCl2‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells

Role of Sirtuins in Tumor Angiogenesis

Potential Role of miRNAs as Theranostic Biomarkers of Epilepsy

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Overexpression of miR‐138‐5p suppresses MnCl₂‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells

Overexpression of miR‐138‐5p suppresses MnCl₂‐induced autophagy by targeting SIRT1 in SH‐SY5Y cells