Oxaliplatin treatment impairs extension of sensory neuron neurites in vitro through miR-204 overexpression

López-González, María José; Soula, Anaïs; Landry, Marc; Favereaux, Alexandre

doi:10.1016/j.neuro.2018.07.009

Cited by 8 publications

(5 citation statements)

References 35 publications

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“…MicroRNAs (miRNAs) are a cluster of highly conserved RNAs that modulate various genes expression by binding to the mRNA 3’UTR of target gene to induce mRNA degradation or translation inhibition 13‐16 . Meanwhile, they are widely expressed in both the central nerve system and peripheral nerve system and have been shown to be involved in regulation of neuronal axon growth ability 17,18 . In Parkinson's disease, miR‐30b shows cytoprotective role via targeting SNCA and inhibiting cell apoptosis 19 .…”

Section: Introductionmentioning

confidence: 99%

“…[13][14][15][16] Meanwhile, they are widely expressed in both the central nerve system and peripheral nerve system and have been shown to be involved in regulation of neuronal axon growth ability. 17,18 In Parkinson's disease, miR-30b shows cytoprotective role via targeting SNCA and inhibiting cell apoptosis. 19 MiR-30b overexpression relieves neuropathic pain.…”

Section: Introductionmentioning

confidence: 99%

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miR‐30b Promotes spinal cord sensory function recovery via the Sema3A/NRP‐1/PlexinA1/RhoA/ROCK Pathway

Wang

et al. 2020

J Cellular Molecular Medi

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR‐30b Promotes spinal cord sensory function recovery via the Sema3A/NRP‐1/PlexinA1/RhoA/ROCK Pathway

Wang

et al. 2020

J Cellular Molecular Medi

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“…While APS mediating miR-204 down-regulation was one of the key findings, the lack of underlying molecular mechanism was the limitation of the current study. Previous studies revealed that abnormal miR-204 expression was correlated to several pathological conditions of human diseases [33,34] and rodent disease models [12,35], indicative of dysregulated transcriptional modulation of miR-204 in diseases. Meanwhile, it was demonstrated that long non-coding RNA or circular RNA may act as competing endogenous RNAs (ceRNAs) to alter the expression level of miR-204 [36][37][38].…”

mentioning

confidence: 99%

Astragalus polysaccharide attenuates metabolic memory-triggered ER stress and apoptosis via regulation of miR-204/SIRT1 axis in retinal pigment epithelial cells

Peng

Tong

et al. 2020

Bioscience Reports

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Background: ‘Metabolic memory’ of early hyperglycaemic environment has been frequently suggested in the progression of diabetic retinopathy (DR). Retinal pigment epithelial (RPE) cells are crucial targets for DR initiation following hyperglycaemia. Astragalus polysaccharides (APS) has been long used as a traditional Chinese medicine in treating diabetes. In the present study, the preventive effects and mechanisms of APS on metabolic memory-induced RPE cell death were investigated. Methods: The expressions of miR-204 and SIRT1 were determined by reverse transcription quantitative PCR (RT-qPCR). Dual luciferase assay was applied to detect the potential targeting effects of miR-204 on SIRT1. SIRT1, ER stress and apoptosis related proteins were monitored using Western blotting. Apoptosis was assessed by TUNEL assay and Annexin V/PI staining followed by flow cytometry analysis. MiR-204 mimics and shSIRT1 were applied for miR-204 overexpression and SIRT1 knockdown, respectively. Results: High glucose exposure induced metabolic memory, which was accompanied with sustained dysregulation of miR-204/SIRT1 axis, high level of ER stress and activation of apoptotic pathway even after replacement with normal glucose. Pre-treatment with APS concentration-dependently reversed miR-204 expression, leading to disinhibition of SIRT1 and alleviation of ER stress-induced apoptosis indicated by decreased levels of p-PERK, p-IRE-1, cleaved-ATF6, Bax, cleaved caspase-12, -9, -3, and increased levels of Bcl-2 and unleaved PARP. The effects of APS on RPE cells were reversed by either miR-204 overexpression or SIRT1 knockdown. Conclusions: We concluded that APS inhibited ER stress and subsequent apoptosis via regulating miR-204/SIRT1 axis in metabolic memory model of RPE cells.

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“…Thus, it is unclear if the association of certain miRNAs with cyTDP43 represents a possible preventive measure or rather promotes neuronal injury. In the case of miR-204, levels are increased in a cellular model of Parkinson's disease (Talepoor Ardakani et al, 2019), it is implicated in optic nerve injury (Wang et al, 2018), and miR-204 overexpression impairs neurite outgrowth (López-González et al, 2018) while inhibition provides neuroprotection (Yan et al, 2019). Ultimately, more research is needed to determine how miRNA profiles change over time, associate with TPD43, and impact ALS progression.…”

Section: Discussionmentioning

confidence: 99%

Cytoplasmic TDP43 Binds microRNAs: New Disease Targets in Amyotrophic Lateral Sclerosis

Paez-Colasante

Figueroa‐Romero

Rumora

et al. 2020

Front. Cell. Neurosci.

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Amyotrophic lateral sclerosis (ALS) is a progressive, fatal, and incurable neurodegenerative disease. Recent studies suggest that dysregulation of gene expression by microRNAs (miRNAs) may play an important role in ALS pathogenesis. The reversible nature of this dysregulation makes miRNAs attractive pharmacological targets and a potential therapeutic avenue. Under physiological conditions, miRNA biogenesis, which begins in the nucleus and includes further maturation in the cytoplasm, involves trans-activation response element DNA/RNA-binding protein of 43 kDa (TDP43). However, TDP43 mutations or stress trigger TDP43 mislocalization and inclusion formation, a hallmark of most ALS cases, that may lead to aberrant protein/miRNA interactions in the cytoplasm. Herein, we demonstrated that TDP43 exhibits differential binding affinity for select miRNAs, which prompted us to profile miRNAs that preferentially bind cytoplasmic TDP43. Using cellular models expressing TDP43 variants and miRNA profiling analyses, we identified differential levels of 65 cytoplasmic TDP43-associated miRNAs. Of these, approximately 30% exhibited levels that differed by more than 3-fold in the cytoplasmic TDP43 models relative to our control model. The hits included both novel miRNAs and miRNAs previously associated with ALS that potentially regulate several predicted genes and pathways that may be important for pathogenesis. Accordingly, these findings highlight specific miRNAs that may shed light on relevant disease pathways and could represent potential biomarkers and reversible treatment targets for ALS.

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Oxaliplatin treatment impairs extension of sensory neuron neurites in vitro through miR-204 overexpression

Cited by 8 publications

References 35 publications

miR‐30b Promotes spinal cord sensory function recovery via the Sema3A/NRP‐1/PlexinA1/RhoA/ROCK Pathway

miR‐30b Promotes spinal cord sensory function recovery via the Sema3A/NRP‐1/PlexinA1/RhoA/ROCK Pathway

Astragalus polysaccharide attenuates metabolic memory-triggered ER stress and apoptosis via regulation of miR-204/SIRT1 axis in retinal pigment epithelial cells

Cytoplasmic TDP43 Binds microRNAs: New Disease Targets in Amyotrophic Lateral Sclerosis

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