Long Non-coding RNA LINC01119 Promotes Neuropathic Pain by Stabilizing BDNF Transcript

Zhang, Le; Feng, Hui; Jin, Yanwu; Zhan, Yufeng; Han, Qi; Zhao, Xin; Li, Peilong

doi:10.3389/fnmol.2021.673669

Cited by 13 publications

(6 citation statements)

References 38 publications

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“…lncRNA CRNDE can upregulate the expression of IL-6 receptors in chronic pain by interacting with miR-136 ( Zhang et al, 2019 ). In addition, lncRNA Linc01119 can interact with embryonic lethal abnormal version-like RNA-binding protein 1 (ELAVL1), upregulate the expression of brain-derived neurotrophic factor (BDNF) at the mRNA and protein levels, and induce chronic pain in the spinal cord and DRG ( Zhang L. et al, 2021 ). In summary, lncRNAs can interact with miRNA or RNA-associated proteins and regulate the different downstream mechanisms involved in chronic pain.…”

Section: The Role Of Lncrnas In the Nervous System And The Pain-signaling Pathwaymentioning

confidence: 99%

Roles of Long Non-coding RNAs in the Development of Chronic Pain

Jian

et al. 2021

Front. Mol. Neurosci.

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Chronic pain, a severe public health issue, affects the quality of life of patients and results in a major socioeconomic burden. Only limited drug treatments for chronic pain are available, and they have insufficient efficacy. Recent studies have found that the expression of long non-coding RNAs (lncRNAs) is dysregulated in various chronic pain models, including chronic neuropathic pain, chronic inflammatory pain, and chronic cancer-related pain. Studies have also explored the effect of these dysregulated lncRNAs on the activation of microRNAs, inflammatory cytokines, and so on. These mechanisms have been widely demonstrated to play a critical role in the development of chronic pain. The findings of these studies indicate the significant roles of dysregulated lncRNAs in chronic pain in the dorsal root ganglion and spinal cord, following peripheral or central nerve lesions. This review summarizes the mechanism underlying the abnormal expression of lncRNAs in the development of chronic pain induced by peripheral nerve injury, diabetic neuropathy, inflammatory response, trigeminal neuralgia, spinal cord injury, cancer metastasis, and other conditions. Understanding the effect of lncRNAs may provide a novel insight that targeting lncRNAs could be a potential candidate for therapeutic intervention in chronic pain.

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Section: The Role Of Lncrnas In the Nervous System And The Pain-signaling Pathwaymentioning

confidence: 99%

Roles of Long Non-coding RNAs in the Development of Chronic Pain

Jian

et al. 2021

Front. Mol. Neurosci.

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“…METTL3, miR-150, and BDNF were stably dysregulated via constructing lentivirus-based vectors by GenePharma (Shanghai, China) and injected with an intrathecal catheter-implantation method [ 18 ]. The treatment timeline was shown in Supplementary Fig.…”

Section: Methodsmentioning

confidence: 99%

METTL3 suppresses neuropathic pain via modulating N6-methyladenosine-dependent primary miR-150 processing

et al. 2022

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Methyltransferase-like 3 (METTL3)-modulated N6-methyladenosine (m6A) was recently identified as an important epigenetic regulation type during RNA processing and contributes to multiple pathological processes. Neuropathic pain (NP) is induced by a lesion of the somatosensory nervous system, and the detailed pathways by which METTL3/m6A regulated to modulate gene dysregulation and enable NP have remained unclear. Therefore, this study investigated the function of METTL3-mediated m6A methylation on miRNA maturation, and investigated how this regulation contributes to NP progression. A rat model characterized with typical NP was established by a spared nerve-injury (SNI) method. By analyzing the expression levels of METTL3 and m6A methylation, we found that METTL3, along with m6A methylation, was dramatically downregulated in NP rats in contrast to the sham ones. Functionally, enhanced METTL3 promoted the m6A methylation in total RNAs and inhibited NP progression, whereas silencing METTL3 suppressed m6A methylation and increased NP severity. Mechanistically, METTL3 accelerated miR-150 maturation via mediating m6A methylation of primiR-150 at locus 498, cooperating with the “m6A reader” YTHDF2. Meanwhile, miR-150 could directly target brain-derived neurotrophic factor (BDNF) mRNA, and the METTL3/miR-150/BDNF regulatory pathway was finally established. Clinically, we proved that serum METTL3 mRNA was also downregulated in Shingles patients with NP, suggesting its diagnostic potential. In conclusion, we demonstrated an essential function of METTL3-regulated N6-methyladenosine during NP progression via modulating primiR-150 maturation. Serum METTL3 could effectively differentiate NP patients from healthy people, and is useful for dynamic monitoring of diseases after treatment. Therefore, the METTL3/miR-150/BDNF pathway may be a promising therapeutic target for NP patients.

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“…While genetic alterations offer a partial explanation for chronic pain, the emerging field of epigenetics provides a more nuanced and dynamic perspective by unraveling the gene expression patterns associated with chronic pain [154,155]. Recent studies revealed that epigenetic mechanisms, including histone acetylation [156], non-coding RNAs [156,157], and DNA methylation [127,158,159], can influence the expression of BDNF (Figure 2, Table 3). These epigenetic modifications may contribute to the pathogenesis and symptomatology of chronic pain.…”

Section: The Epigenetic Regulation Of Bdnf Expression In Chronic Painmentioning

confidence: 99%

The Role of the Brain-Derived Neurotrophic Factor in Chronic Pain: Links to Central Sensitization and Neuroinflammation

Xiong,

Hendrix,

Schabrun

et al. 2024

Biomolecules

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Chronic pain is sustained, in part, through the intricate process of central sensitization (CS), marked by maladaptive neuroplasticity and neuronal hyperexcitability within central pain pathways. Accumulating evidence suggests that CS is also driven by neuroinflammation in the peripheral and central nervous system. In any chronic disease, the search for perpetuating factors is crucial in identifying therapeutic targets and developing primary preventive strategies. The brain-derived neurotrophic factor (BDNF) emerges as a critical regulator of synaptic plasticity, serving as both a neurotransmitter and neuromodulator. Mounting evidence supports BDNF’s pro-nociceptive role, spanning from its pain-sensitizing capacity across multiple levels of nociceptive pathways to its intricate involvement in CS and neuroinflammation. Moreover, consistently elevated BDNF levels are observed in various chronic pain disorders. To comprehensively understand the profound impact of BDNF in chronic pain, we delve into its key characteristics, focusing on its role in underlying molecular mechanisms contributing to chronic pain. Additionally, we also explore the potential utility of BDNF as an objective biomarker for chronic pain. This discussion encompasses emerging therapeutic approaches aimed at modulating BDNF expression, offering insights into addressing the intricate complexities of chronic pain.

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Long Non-coding RNA LINC01119 Promotes Neuropathic Pain by Stabilizing BDNF Transcript

Cited by 13 publications

References 38 publications

Roles of Long Non-coding RNAs in the Development of Chronic Pain

Roles of Long Non-coding RNAs in the Development of Chronic Pain

METTL3 suppresses neuropathic pain via modulating N6-methyladenosine-dependent primary miR-150 processing

The Role of the Brain-Derived Neurotrophic Factor in Chronic Pain: Links to Central Sensitization and Neuroinflammation

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