&lt;p&gt;Intraneural Application of microRNA-1 Mimetic Nucleotides Does Not Resolve Neuropathic Pain After Chronic Constriction Injury in Rats&lt;/p&gt;

Kuebart, Anne; Wollborn, Verena; Huhn, Ragnar; Hermanns, Henning; Werdehausen, Robert; Brandenburger, Timo

doi:10.2147/jpr.s266937

Cited by 3 publications

(3 citation statements)

References 34 publications

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“…The authors attributed such treatment failure to insufficient inhibition of miR‐1 for Cx43 via intraneural injection. Alternatively, there were regulatory mechanisms for Cx43 in vivo other than miR‐1 90 . However, miR‐1 in the DRG was DE according to peripheral nerve injury type.…”

Section: Studying Mirna Neuropathic Pain Mechanismsmentioning

confidence: 98%

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The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review

Jiang

Wang

et al. 2022

Clinical Laboratory Analysis

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Background Non‐coding RNAs (ncRNAs) are involved in neuropathic pain development. Herein, we systematically searched for neuropathic pain‐related ncRNAs expression changes, including microRNAs (miRNAs), long non‐coding RNAs (lncRNAs), and circular non‐coding RNAs (circRNAs). Methods We searched two databases, PubMed and GeenMedical, for relevant studies. Results Peripheral nerve injury or noxious stimuli can induce extensive changes in the expression of ncRNAs. For example, higher serum miR‐132‐3p, ‐146b‐5p, and ‐384 was observed in neuropathic pain patients. Either sciatic nerve ligation, dorsal root ganglion (DRG) transaction, or ventral root transection (VRT) could upregulate miR‐21 and miR‐31 while downregulating miR‐668 and miR‐672 in the injured DRG. lncRNAs, such as early growth response 2‐antisense‐RNA (Egr2‐AS‐RNA) and Kcna2‐AS‐RNA, were upregulated in Schwann cells and inflicted DRG after nerve injury, respectively. Dysregulated circRNA homeodomain‐interacting protein kinase 3 (circHIPK3) in serum and the DRG, abnormally expressed lncRNAs X‐inactive specific transcript (XIST), nuclear enriched abundant transcript 1 (NEAT1), small nucleolar RNA host gene 1 (SNHG1), as well as ciRS‐7, zinc finger protein 609 (cirZNF609), circ_0005075, and circAnks1a in the spinal cord were suggested to participate in neuropathic pain development. Dysregulated miRNAs contribute to neuropathic pain via neuroinflammation, autophagy, abnormal ion channel expression, regulating pain‐related mediators, protein kinases, structural proteins, neurotransmission excitatory–inhibitory imbalances, or exosome miRNA‐mediated neuron–glia communication. In addition, lncRNAs and circRNAs are essential in neuropathic pain by acting as antisense RNA and miRNA sponges, epigenetically regulating pain‐related molecules expression, or modulating miRNA processing. Conclusions Numerous dysregulated ncRNAs have been suggested to participate in neuropathic pain development. However, there is much work to be done before ncRNA‐based analgesics can be clinically used for various reasons such as conservation among species, proper delivery, stability, and off‐target effects.

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Section: Studying Mirna Neuropathic Pain Mechanismsmentioning

confidence: 98%

“…Alternatively, there were regulatory mechanisms for Cx43 in vivo other than miR‐1. 90 However, miR‐1 in the DRG was DE according to peripheral nerve injury type. CCI, pSNL, and sural nerve injury downregulated miR‐1.…”

Section: Studying Mirna Neuropathic Pain Mechanismsmentioning

confidence: 99%

The etiological roles of miRNAs, lncRNAs, and circRNAs in neuropathic pain: A narrative review

Jiang

Wang

et al. 2022

Clinical Laboratory Analysis

View full text Add to dashboard Cite

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“…Strategies such as the use of PLGA particles (mentioned above) that have shown selectivity and efficacy for a neuropathic pain model [ 152 ] are worth investigating further. Nonetheless, their therapeutic potential remains narrow as efficacy of tackling ncRNAs has only been proven in preclinical studies via intrathecal administration [ 44 , 93 , 119 , 126 , 136 , 137 , 140 ] which, additionally, seems to lead to contradictory findings [ 154 ].…”

Section: Non-coding Rnas and Painmentioning

confidence: 99%

DNA Methylation and Non-Coding RNAs during Tissue-Injury Associated Pain

Irfan

Febrianto

Sharma

et al. 2022

IJMS

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While about half of the population experience persistent pain associated with tissue damages during their lifetime, current symptom-based approaches often fail to reduce such pain to a satisfactory level. To provide better patient care, mechanism-based analgesic approaches must be developed, which necessitates a comprehensive understanding of the nociceptive mechanism leading to tissue injury-associated persistent pain. Epigenetic events leading the altered transcription in the nervous system are pivotal in the maintenance of pain in tissue injury. However, the mechanisms through which those events contribute to the persistence of pain are not fully understood. This review provides a summary and critical evaluation of two epigenetic mechanisms, DNA methylation and non-coding RNA expression, on transcriptional modulation in nociceptive pathways during the development of tissue injury-associated pain. We assess the pre-clinical data and their translational implication and evaluate the potential of controlling DNA methylation and non-coding RNA expression as novel analgesic approaches and/or biomarkers of persistent pain.

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