Small RNA-Seq reveals novel miRNAs shaping the transcriptomic identity of rat brain structures

Soula, Anaïs; Valere, Mélissa; López-González, María-José; Ury-Thiery, Vicky; Groppi, Alexis; Landry, Marc; Nikolski, Macha; Favereaux, Alexandre

doi:10.26508/lsa.201800018

Cited by 6 publications

(5 citation statements)

References 123 publications

(132 reference statements)

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“…The miR‐344g was found to be differentially expressed in exosomes from the vascular smooth muscle cell calcification model (Pan et al, 2020). Furthermore, the involvement of miR‐344g in spinal cord development and pain mechanisms has been previously investigated (Soula et al, 2018). Subcutaneous injections of MTX are known to be in line with a mild amount of pain (Bechard et al, 2014; Zhou et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Differentially expressed miRNAs in bone after methotrexate treatment

Zhang

Liu

Pillman

et al. 2021

Journal Cellular Physiology

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Previous studies have shown that administration of antimetabolite methotrexate (MTX) caused a reduced trabecular bone volume and increased marrow adiposity (bone/fat switch), for which the underlying molecular mechanisms and recovery potential are unclear. Altered expression of microRNAs (miRNAs) has been shown to be associated with dysregulation of osteogenic and/or adipogenic differentiation by disrupting target gene expression. First, the current study confirmed the bone/fat switch following MTX treatment in precursor cell culture models in vitro. Then, using a rat intensive 5-once daily MTX treatment model, this study aimed to identify miRNAs associated with bone damage and recovery (in a time course over Days 3, 6, 9, and 14 after the first MTX treatment). RNA isolated from bone samples of treated and control rats were subjected to miRNA array and reverse transcriptionpolymerase chain reaction validation, which identified five upregulated miRNA candidates, namely, miR-155-5p, miR-154-5p, miR-344g, miR-6215, and miR-6315.Target genes of these miRNAs were predicted using TargetScan and miRDB. Then, the protein-protein network was established via STRING database, after which the miRNA-key messenger RNA (mRNA) network was constructed by Cytoscape.Functional annotation and pathway enrichment analyses for miR-6315 were performed by DAVID database. We found that TGF-β signaling was the most significantly enriched pathway and subsequent dual-luciferase assays suggested that Smad2 was the direct target of miR-6315. Our current study showed that miR-6315 might be a vital regulator involved in bone and marrow fat formation. Also, this study constructed a comprehensive miRNA-mRNA regulatory network, which may contribute to the pathogenesis/prognosis of MTX-associated bone loss and bone marrow adiposity.

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Section: Discussionmentioning

confidence: 99%

Differentially expressed miRNAs in bone after methotrexate treatment

Zhang

Liu

Pillman

et al. 2021

Journal Cellular Physiology

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“…While the molecular mechanisms of mRNA spatial distributions are well-studied, those of ncRNAs are still largely unknown. Emerging evidence indicates that miRNAs specifically localize within the brain, brain regions, and brain cells [ 31 , 32 , 33 , 34 , 35 , 36 , 37 ], but also in the subcellular compartments, including the axon [ 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 ]. Here, we briefly summarize the current knowledge of miRNA spatial distribution and associated transport mechanism within the axon.…”

Section: In the Right Place: Mirnas Are Translocated To Developingmentioning

confidence: 99%

In the Right Place at the Right Time: miRNAs as Key Regulators in Developing Axons

Corradi

Baudet

2020

IJMS

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During neuronal circuit formation, axons progressively develop into a presynaptic compartment aided by extracellular signals. Axons display a remarkably high degree of autonomy supported in part by a local translation machinery that permits the subcellular production of proteins required for their development. Here, we review the latest findings showing that microRNAs (miRNAs) are critical regulators of this machinery, orchestrating the spatiotemporal regulation of local translation in response to cues. We first survey the current efforts toward unraveling the axonal miRNA repertoire through miRNA profiling, and we reveal the presence of a putative axonal miRNA signature. We also provide an overview of the molecular underpinnings of miRNA action. Our review of the available experimental evidence delineates two broad paradigms: cue-induced relief of miRNA-mediated inhibition, leading to bursts of protein translation, and cue-induced miRNA activation, which results in reduced protein production. Overall, this review highlights how a decade of intense investigation has led to a new appreciation of miRNAs as key elements of the local translation regulatory network controlling axon development.

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“…Among the actors that can regulate local protein translation, microRNAs (miRNAs) control various forms of HSP (Mellios et al , 2011 ; Tognini et al , 2011 ; Fiore et al , 2014 ; Letellier et al , 2014 ; Rajman et al , 2017 ; Dubes et al , 2019 ; Silva et al , 2019 ). These small noncoding RNAs hybridize to the 3' UTR of multiple target mRNAs and inhibit protein synthesis through translational repression or destabilization of the transcripts (Filipowicz et al , 2008 ; Friedman et al , 2009 ; Soula et al , 2018 ). In neurons, miRNAs can be found in proximity of synapses where they likely respond to activity change and in turn regulate synaptic plasticity (Schratt, 2009 ; Letellier et al , 2014 ; Sambandan et al , 2017 ; Park et al , 2019 ).…”

Section: Introductionmentioning

confidence: 99%

miR‐124‐dependent tagging of synapses by synaptopodin enables input‐specific homeostatic plasticity

et al. 2022

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Homeostatic synaptic plasticity is a process by which neurons adjust their synaptic strength to compensate for perturbations in neuronal activity. Whether the highly diverse synapses on a neuron respond uniformly to the same perturbation remains unclear. Moreover, the molecular determinants that underlie synapse‐specific homeostatic synaptic plasticity are unknown. Here, we report a synaptic tagging mechanism in which the ability of individual synapses to increase their strength in response to activity deprivation depends on the local expression of the spine‐apparatus protein synaptopodin under the regulation of miR‐124. Using genetic manipulations to alter synaptopodin expression or regulation by miR‐124, we show that synaptopodin behaves as a “postsynaptic tag” whose translation is derepressed in a subpopulation of synapses and allows for nonuniform homeostatic strengthening and synaptic AMPA receptor stabilization. By genetically silencing individual connections in pairs of neurons, we demonstrate that this process operates in an input‐specific manner. Overall, our study shifts the current view that homeostatic synaptic plasticity affects all synapses uniformly to a more complex paradigm where the ability of individual synapses to undergo homeostatic changes depends on their own functional and biochemical state.

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Small RNA-Seq reveals novel miRNAs shaping the transcriptomic identity of rat brain structures

Abstract: Small RNA-Seq of the rat central nervous system reveals known and novel miRNAs specifically regulated in brain structures and correlated with the expression of their predicted target genes, suggesting a critical role in the transcriptomic identity of brain structures.

Cited by 6 publications

References 123 publications

Differentially expressed miRNAs in bone after methotrexate treatment

Differentially expressed miRNAs in bone after methotrexate treatment

In the Right Place at the Right Time: miRNAs as Key Regulators in Developing Axons

miR‐124‐dependent tagging of synapses by synaptopodin enables input‐specific homeostatic plasticity

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