MicroRNA and chronic pain: From mechanisms to therapeutic potential

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

doi:10.1016/j.pharmthera.2017.06.001

Cited by 92 publications

(75 citation statements)

References 175 publications

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“…Recently, more and more roles of miRNAs in neuropathic pain have been reported. [28][29][30] Currently, in this study, we observed a suppressive role of miR-150 in neuropathic pain development in CCI rats. MiR-150 was downregulated in CCI rat models and it could alleviate neuropathic pain development.…”

Section: Discussionmentioning

confidence: 52%

MiR‐150 alleviates neuropathic pain via inhibiting toll‐like receptor 5

Shi

et al. 2017

J of Cellular Biochemistry

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MicroRNAs (miRNAs) are reported as vital participators in the pathophysiological course of neuropathic pain. However, the underlying mechanisms of the functional roles of miRNAs in neuropathic pain are largely unknown. This study was designed to explore the potential role of miR-150 in regulating the process of neuropathic pain in a rat model established by chronic sciatic nerve injury (CCI). Overexpression of miR-150 greatly alleviated neuropathic pain development and reduced inflammatory cytokine expression, including COX-2, interleukin IL-6, and tumor necrosis factor (TNF)-α in CCI rats. By bioinformatic analysis, 3′-untranslated region (UTR) of Tolllike receptor (TLR5) was predicted to be a target of miR-150. TLR5 commonly serves as an important regulator of inflammation. Overexpression of miR-150 significantly suppressed the expression of TLR5 in vitro and in vivo. Furthermore, upregulation of TLR5 decreased the miR-150 expression and downregulation of TLR5 increased miR-150, respectively. Overexpression of TLR5 significantly reversed the miR-150-induced suppressive effects on neuropathic pain. In conclusion, our current study indicates that miR-150 may inhibit neuropathic pain development of CCI rats through inhibiting TLR5-mediated neuroinflammation. Our findings suggest that miR-150 may provide a novel therapeutic target for neuropathic pain treatment. K E Y W O R D Schronic constriction injury, miR-150, neuropathic pain, TLR5

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Section: Discussionmentioning

confidence: 52%

MiR‐150 alleviates neuropathic pain via inhibiting toll‐like receptor 5

Shi

et al. 2017

J of Cellular Biochemistry

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“…17 While, more recent studies suggest that m 6 A modification could mark primary miRNA (pri-miRNA) for processing by recognizing a microprocessor complex subunit DGCR8. 18,19 Given the importance of miRNAs in the pathogenesis of nociceptive sensitization, 20 we hypothesized that METTL3 may regulate CFA-induced inflammatory pain via regulating pri-miRNA processing in an m 6 A-dependent manner. To test the hypothesis, we first assessed whether DGCR8 coprecipitates with methylated RNA.…”

Section: Mettl3-dependent M 6 a Modification Modulates The Processimentioning

confidence: 99%

METTL3 regulates inflammatory pain by modulating m⁶A‐dependent pri‐miR‐365‐3p processing

Zhang¹,

Wang

Peng

et al. 2019

The FASEB Journal

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N6‐methyladenosine (m6A) modification in RNA has been implicated in diverse biological processes. However, very little is currently known about its role in nociceptive modulation. Here, we found that the level of spinal m6A modification was significantly increased in a mouse model of Complete Freund's Adjuvant (CFA)‐induced chronic inflammatory pain, which was accompanied with the augmentation of methyltransferase‐like 3 (METTL3) expression in the spinal cord. Knockdown of spinal METTL3 prevented and reversed CFA‐induced pain behaviors and spinal neuronal sensitization. In contrast, overexpression of spinal METTL3 produced pain behaviors and neuronal sensitization in naive mice. Moreover, we found that METTL3 positively modulated the pri‐miR‐65‐3p processing in a microprocessor protein DiGeorge critical region 8‐dependent manner. Collectively, our findings reveal an important role of METTL3‐mediated m6A modification in nociceptive sensitization and provide a novel perspective on m6A modification in the development of pathological pain.

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“…microRNAs belong to a kind of small non‐coding RNAs that can modulate gene expression through translational inhibition or mRNA degradation (Bartel, ). Recently, it has been reported that miRNAs can regulate nervous system genes and they can lead to neuronal network plasticity (Lopez‐Gonzalez, Landry, & Favereaux, ). miR‐150 can relieve neuropathic pain by targeting toll‐like receptor 5 (Ji, Lu, & Huang, ).…”

Section: Introductionmentioning

confidence: 99%

Effects of XIST/miR‐137 axis on neuropathic pain by targeting TNFAIP1 in a rat model

Zhao

Xia

et al. 2017

Journal Cellular Physiology

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Non-coding RNAs have been reported to participate in the pathophysiology of neuropathic pain. The objective of our study was to investigate the biological role of XIST in neuropathic pain development. In our study, we identify and validate that lncRNA XIST was markedly increased and miR-137 was significantly decreased in chronic constriction injury (CCI) rats. XIST silencing alleviated pain behaviors including both mechanical and thermal hyperalgesia in the CCI rats. XIST was predicted to interact with miR-137 by bioinformatics technology and dual-luciferase reporter assays confirmed the correlation between XIST and miR-137. miR-137 was negatively modulated by XIST and upregulation of miR-137 greatly reduced neuropathic pain development in CCI rats. Moreover, we observed that tumor necrosis factor alpha-induced protein 1 (TNFAIP1) was enhanced in CCI rats and 3'-untranslated region (UTR) of TNFAIP1 was exhibited to be a target of miR-137 by bioinformatics prediction. TNFAIP1 can act as a crucial inflammation regulator by activating NF-kB activity. Overexpression of miR-137 significantly suppressed TNFAIP1 both in vitro and in vivo. Furthermore, upregulation of XIST reversed the inhibitory role of miR-137 in neuropathic pain development by inhibiting TNFAIP1. In conclusion, our current study indicates that XIST can positively regulate neuropathic pain in rats through regulating the expression of miR-137 and TNFAIP1. Our results imply that XIST/miR-137/TNFAIP1 axis may serve as a novel therapeutic target in neuropathic pain.

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MicroRNA and chronic pain: From mechanisms to therapeutic potential

Cited by 92 publications

References 175 publications

MiR‐150 alleviates neuropathic pain via inhibiting toll‐like receptor 5

MiR‐150 alleviates neuropathic pain via inhibiting toll‐like receptor 5

METTL3 regulates inflammatory pain by modulating m⁶A‐dependent pri‐miR‐365‐3p processing

Effects of XIST/miR‐137 axis on neuropathic pain by targeting TNFAIP1 in a rat model

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MicroRNA and chronic pain: From mechanisms to therapeutic potential

Cited by 92 publications

References 175 publications

MiR‐150 alleviates neuropathic pain via inhibiting toll‐like receptor 5

MiR‐150 alleviates neuropathic pain via inhibiting toll‐like receptor 5

METTL3 regulates inflammatory pain by modulating m6A‐dependent pri‐miR‐365‐3p processing

Effects of XIST/miR‐137 axis on neuropathic pain by targeting TNFAIP1 in a rat model

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METTL3 regulates inflammatory pain by modulating m⁶A‐dependent pri‐miR‐365‐3p processing