LncRNA CRNDE exacerbates neuropathic pain in chronic constriction injury-induced(CCI) rats through regulating miR-146a-5p/WNT5A pathway

Zhang, Qiangze; Zhu, Dongxia; Li, Qiang

doi:10.1080/21655979.2021.1972901

Cited by 14 publications

(4 citation statements)

References 49 publications

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“… 330 , 331 Some molecular regulators, such as SFRP1, LPAR3, miR-26a-5p and LncCRNDE, jointly control Wnt/β-catenin signaling-mediated neuropathic pain. 331 – 334 A recent study demonstrated that GPR177 promotes the secretion of Wnt5a from A-fiber DRG neurons, which further enhances rapid currents of TRPV1+ nociceptive DRG neurons. 335 This finding has strongly revealed the functions of intercellular communications via Wnt/β-catenin signaling during neuropathic pain progression.…”

Section: Molecular Mechanisms Of Pain Modulationmentioning

confidence: 99%

Pathology of pain and its implications for therapeutic interventions

Cao,

Xu,

Shi

et al. 2024

Sig Transduct Target Ther

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Pain is estimated to affect more than 20% of the global population, imposing incalculable health and economic burdens. Effective pain management is crucial for individuals suffering from pain. However, the current methods for pain assessment and treatment fall short of clinical needs. Benefiting from advances in neuroscience and biotechnology, the neuronal circuits and molecular mechanisms critically involved in pain modulation have been elucidated. These research achievements have incited progress in identifying new diagnostic and therapeutic targets. In this review, we first introduce fundamental knowledge about pain, setting the stage for the subsequent contents. The review next delves into the molecular mechanisms underlying pain disorders, including gene mutation, epigenetic modification, posttranslational modification, inflammasome, signaling pathways and microbiota. To better present a comprehensive view of pain research, two prominent issues, sexual dimorphism and pain comorbidities, are discussed in detail based on current findings. The status quo of pain evaluation and manipulation is summarized. A series of improved and innovative pain management strategies, such as gene therapy, monoclonal antibody, brain-computer interface and microbial intervention, are making strides towards clinical application. We highlight existing limitations and future directions for enhancing the quality of preclinical and clinical research. Efforts to decipher the complexities of pain pathology will be instrumental in translating scientific discoveries into clinical practice, thereby improving pain management from bench to bedside.

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Section: Molecular Mechanisms Of Pain Modulationmentioning

confidence: 99%

Pathology of pain and its implications for therapeutic interventions

Cao,

Xu,

Shi

et al. 2024

Sig Transduct Target Ther

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“…The capsaicin receptor (TRPV1) in mature neurons functions in transducing injurious signals and generating pain as a heat‐sensitive ion channel 14 ; hence, lower TRPV1 expression can effectively inhibit NP progression. 15 WNT5a belongs to the Wingless‐type MMTV integration site family, 16 acting on neurons through the β‐catenin‐independent WNT signaling pathway, and has been reported to be involved in NP development. 17 Recent research indicates that the activation of TRPV1 by WNT5a is essential for NP formation, which is regulated by GPR177, 18 which was an intriguing factor in this study since studies on exploring pathways and regulatory mechanisms in this process are scarce.…”

Section: Introductionmentioning

confidence: 99%

Silencing of FTO inhibits oxidative stress to relieve neuropathic pain by m6A modification of GPR177

Liu,

Song

et al. 2024

Immunity Inflam & Disease

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BackgroundNeuropathic pain (NP) is a challenging health condition owing to its complex nature and associated multiple etiologies. The occurrence of NP involves the abnormal activity of neurons mediated by oxidative stress (OS). Previous research has demonstrated that m6A methylation plays a role in the regulatory pathway of NP. This study aimed to investigate the specific molecular pathways through which m6A methylation modifiers alleviate NP.MethodsFor this purpose, an NO rat model was developed via spared nerve injury (SNI), followed by quantifying the animal's pain assessment via paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). The OS in SNI rats was evaluated by measuring reactive oxygen species, superoxide dismutase, and catalase (CAT) in spinal cord tissues. Moreover, quantitative‐real‐time polymerase chain reaction and western blot analysis were employed for detecting fat mass and obesity‐associated (FTO) and GPR177 levels, while m6A levels of GPR117 were analyzed via MeRIP.ResultsThe results indicated an enhanced OS with highly expressed FTO in spinal cord tissue samples, where knocking down Fto effectively relieved NP and OS in SNI rats. Mechanistic investigations revealed that Fto‐mediated reduction of Grp177 m6A modification was involved in the WNT5a/TRPV1 axis‐mediated OS remission of NP. Moreover, in vitro experiment results indicated that YTHDF2 was an important m6A methylated reading protein for this process.ConclusionsFto silencing leads to increased m6A methylation of Grp177 through a YTHDF2‐dependent mechanism, resulting in decreased Grp177 stability and ultimately reducing NP in rats by OS suppression.

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“…Aberrant expression of lncRNAs is associated with human diseases, particularly in the nervous system, and has been postulated as a therapeutic biomarker for neurogenic diseases. For instance, lncRNA MALAT1 [26], FIRRE [35], PVT1 [42], and CENDES [44] were identified to be involved in the pathological process of NP. Five prime to XIST (FTX) is a highly conserved LncRNA, located on chromosome Xq13.2, containing 2300 nucleotides.…”

Section: Introductionmentioning

confidence: 99%

LncRNA FTX ameliorates neuropathic pain by targeting miR-320a in a rat model of chronic constriction injury

Lu¹,

Zhang²,

Li³

2023

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Introduction: Long non-coding RNAs (lncRNAs) participate in the process of neuropathic pain (NP). Herein, the goal of this research was to examine the roles of lncRNA five prime to XIST (FTX) in influencing chronic constriction injury (CCI)-induced NP. Material and methods: We have established a rat CCI model to simulate NP in vivo. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect mRNA levels of FTX, microRNA (miR)-320a, and runt-related transcription factor 2 (RUNX2) in the spinal cord. This was followed by subsequent regulation of FTX or miR-320a levels in vivo by intrathecal injection of overexpression FTX or miR-320a mimic lentivirus. The behaviour of rat NP was assessed by the paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). Enzyme-linked immunosorbent assay (ELISA) was used to assess the secretion of pro-inflammatory and anti-inflammatory factors in the spinal cord tissue. A correlation between miR-320a and FTX or RUNX2 was validated by luciferase reporter.Results: FTX levels were reduced in CCI rats (p < 0.05), and miR-320a was a direct target of FTX. Overexpression of FTX typically reduced PWL and PWT as well as neuroinflammation thus alleviating NP (p < 0.05). However, increasing miR-320a reversed the alleviation of FTX on NP, increased PWL and PWT, and promoted neuroinflammation (p < 0.05). Additionally, RUNX2, which is a miR-320a target gene, was significantly repressed in CCI rats and its expression was increased by FTX, however, this increase was attenuated by elevated miR-320a (p < 0.05). Conclusions: In the CCI-induced NP rat model, FTX attenuates NP and neuroinflammation by regulating the miR-320a/ RUNX2 axis. This provides a new vision for NP treatment.

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LncRNA CRNDE exacerbates neuropathic pain in chronic constriction injury-induced(CCI) rats through regulating miR-146a-5p/WNT5A pathway

Cited by 14 publications

References 49 publications

Pathology of pain and its implications for therapeutic interventions

Pathology of pain and its implications for therapeutic interventions

Silencing of FTO inhibits oxidative stress to relieve neuropathic pain by m6A modification of GPR177

LncRNA FTX ameliorates neuropathic pain by targeting miR-320a in a rat model of chronic constriction injury

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