Long noncoding RNA MRAK009713 is a novel regulator of neuropathic pain in rats

Li, Guilin; Jiang, Huaide; Zheng, Chaoran; Zhu, Guo‐Qing; Xu, Yurong; Xuan, Shi‐Ying; Wu, Bing; Guo, Jingjing; Zhu, Sencun; Zhan, Yuting; Lin, Weijian; Ding, Rui; Zhang, Chunping; Liu, Shuangmei; Zou, Lifang; Yi, Zhihua; Liang, Shangdong

doi:10.1097/j.pain.0000000000001013

Cited by 61 publications

(66 citation statements)

References 40 publications

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“…Emerging evidence indicates that lncRNAs are deregulated and play important roles in the development of neuropathic pain [4,5]. For example, Li et al [22] reported that lncRNA MRAK009713 expression was markedly increased in CCI rats, and siRNA against MRAK009713 significantly inhibited the nociceptive P2X3 expression and thus reduced both mechanical and thermal hyperalgesia in the CCI rats. Gm14461 was highly expressed in injured DRG 6 days following peripheral nerve injury in mice with neuropathic pain, suggesting the potential involvement of Gm14461 in regulating neuropathic pain [11].…”

Section: Discussionmentioning

confidence: 99%

Effects of long non-coding RNA Gm14461 on pain transmission in trigeminal neuralgia

Yan

Zhu

et al. 2020

J Inflamm

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Background: This study aims to investigate the role of long non-coding RNA Gm14461 in regulating pain transmission in trigeminal neuralgia (TN). The mouse TN model was produced by chronic constriction injury of the infraorbital nerve (CCI-ION). The values of mechanical withdrawal threshold (MWT) were measured to assess the nociception of mice at different times after CCI-ION surgery (0, 1, 3, 5, 7, 9, 11, 13, 15 d). The primary mouse trigeminal ganglion neurons (TGNs) were isolated from C57BL/6 J mice and treated with TNF-α to mimic a TN cellular model. The expression of Gm14461, TNF-α, IL-1β, and IL-6 was examined using qRT-PCR. The protein levels of CGRP and P2X3/7 receptor were measured using western blot.Results: Gm14461 expression was increased in trigeminal ganglia (TGs) of TN mice on the operation side. Furthermore, Gm14461 knockdown in TGs increased, whereas Gm14461 overexpression decreased MWT in TN mice. Moreover, Gm14461 knockdown downregulated, whereas Gm14461 overexpression upregulated mRNA levels of TNF-α, IL-1β, and IL-6 and protein levels of CGRP and P2X3/7 receptor in TGs from TN mice. In vitro assay showed that Gm14461 was upregulated by TNF-α, IL-1β, and IL-6. Additionally, Gm14461 knockdown decreased protein levels of CGRP and P2X3/7 receptor in TNF-α-treated TGNs, whereas Gm14461 overexpression exerted the opposite effect.Conclusion: Gm14461 promoted pain transmission (reduced MWT value) in a CCI-ION-induced mouse TN model. The underlying mechanisms might involve the regulation of pro-inflammatory cytokines, CGRP and P2X3/7 receptor.

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Section: Discussionmentioning

confidence: 99%

Effects of long non-coding RNA Gm14461 on pain transmission in trigeminal neuralgia

Yan

Zhu

et al. 2020

J Inflamm

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“…Next, the underlying mechanism of GClnc1 was revealed. GClnc1 was mainly located in bladder cancer nuclei, and the catRapid online tool was used to predict the interaction GClnc1 and proteins (39)(40)(41). Results showed that LIN28B can bind to GClnc1 through catRapid prediction.…”

Section: Discussionmentioning

confidence: 99%

LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC

Zhuang

et al. 2019

FASEB j.

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Various studies demonstrate that long noncoding RNAs (IncRNAs) act as oncogenes or tumor suppressors in cancer. However, the function of IncRNAs in bladder cancer still remains largely unknown. In this study, we identified an IncRNA, gastric cancer–associated IncRNA1 (GClnc1), which was in high abundance in bladder cancer tissues and its expression was related to poor survival rates in patients with bladder cancer. In vitro and in vivo assays showed that GClnc1 significantly promoted cell proliferation, metastasis, and invasiveness in bladder cancer. Mechanistically, we first found that GClnc1 bound to LIN28B and promoted the expression of myelocytomatosis proto‐oncogene (MYC) through the LIN28B/let‐7a/MYC pathway. In short, GClnc1 is clinically, functionally, and mechanistically oncogenic in bladder cancer. GClnc1 may be a potential target for treating patients with bladder cancer.—Zhuang, C., Ma, Q., Zhuang, C., Ye, J., Zhang, F., Gui, Y. LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC. FASEB J. 33, 11045–11059 (2019). http://www.fasebj.org

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“…In Hirschsprung's disease (HSCR), apoptotic neurons can inhibit apoptosis in non-apoptotic cells by secreting extracellular bodies containing high levels of HN12-lncRNA [24]. In chronic compressive injury (CCI), lncRNA MRAK009713 is a major regulator of neuropathic pain in rats and is significantly increased in CCI rats with enhanced pain behavior [25]. Interestingly, abnormal expression of various lncRNAs makes much sense in ischemic brain injury.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine had neuroprotective effects on hippocampal neuronal cells via targeting lncRNA SHNG16 mediated microRNA-10b-5p/BDNF axis

et al. 2020

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Dexmedetomidine (DEX), a highly selective alpha2 adrenergic receptor agonist, is a commonly used anesthetic drug in surgical procedures. Previous studies have indicated that DEX exerts neuroprotective effects while the detailed mechanism has not been fully elucidated. Here, we aim to study the role of lncRNA SHNG16 in DEX-induced brain protection and its underlying molecular mechanism. The rats underwent middle cerebral artery occlusion (MCAO) surgery and oxygen-glucose deprivation (OGD)-treated HT22 hippocampal neurons were treated with DEX, respectively. CCK8 was used to evaluate cell viability. sh-SHNG16 as well as miR-10b-5p mimics were transfected into hippocampal neurons to further explore the bio-function of SNHG16 and miR-10b-5p in vitro. Furthermore, the interactions between SHNG16 and miR-10b-5p, miR-10b-5p and BDNF gene were confirmed by dual-luciferase report assay. Our data revealed that DEX attenuated neurological damage of the MCAO rats and also increased the cell viability of the neurons significantly. Besides, expression of SHNG16 and BDNF were both downregulated while miR-10b-5p was upregulated in MCAO brain tissues or OGD treated neurons. DEX inhibited miR-10b-5p expression but increased SHNG16 and BDNF levels with a dosage effect. After transfection with sh-SHNG16 or miR-10b-5p mimics, the expression of BDNF protein was downregulated, accompanied with decreased neuron viability. Dual-luciferase assay showed that SHNG16 targeted on miR-10b-5p, which also could bind directly to the 3′-UTR sites of BDNF and negatively regulate its expression. In conclusion, DEX exerts neuroprotective in ischemic stroke via improving neuron damage, the underlying mechanism may be upregulating SHNG16 and BDNF via sponging miR-10b-5p.

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Long noncoding RNA MRAK009713 is a novel regulator of neuropathic pain in rats

Cited by 61 publications

References 40 publications

Effects of long non-coding RNA Gm14461 on pain transmission in trigeminal neuralgia

Effects of long non-coding RNA Gm14461 on pain transmission in trigeminal neuralgia

LncRNA GClnc1 promotes proliferation and invasion of bladder cancer through activation of MYC

Dexmedetomidine had neuroprotective effects on hippocampal neuronal cells via targeting lncRNA SHNG16 mediated microRNA-10b-5p/BDNF axis

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