MicroRNA-142-3p relieves neuropathic pain by targeting high mobility group box 1

Zhang, Yang; Mou, Junying; Cao, Li; Huang, Hongjuan; Bao, Huihui

doi:10.3892/ijmm.2017.3222

Cited by 24 publications

(20 citation statements)

References 64 publications

(78 reference statements)

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“…Knockdown of miR-423-5p can enhance glioma stem cells sensitivity to apigenin via regulating the mitochondrial pathway [35]. In ovarian cancer, miR-423-5p can serve as an indicator, which can repress proliferation and invasion [36]. In addition, lncRNA AFAP1-AS1 can act as a ceRNA of miR-423-5p, which can facilitate nasopharyngeal carcinoma by regulating Rho/Rac pathway [37].…”

Section: Discussionmentioning

confidence: 99%

Loss of SNHG4 Attenuated Spinal Nerve Ligation-Triggered Neuropathic Pain through Sponging miR-423-5p

Pan

Shen

Huang

et al. 2020

Mediators of Inflammation

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Neuropathic pain is an intractable comorbidity of spinal cord injury. Increasing noncoding RNAs have been implicated in neuropathic pain development. lncRNAs have been recognized as significant regulators of neuropathic pain. lncRNA Small Nucleolar RNA Host Gene 4 (SNHG4) is associated with several tumors. However, the molecular mechanisms of SNHG4 in neuropathic pain remain barely documented. Here, we evaluated the function of SNHG4 in spinal nerve ligation (SNL) rat models. We observed that SNHG4 was significantly upregulated in SNL rat. Knockdown of SNHG4 was able to attenuate neuropathic pain progression via regulating behaviors of neuropathic pain including mechanical and thermal hyperalgesia. Moreover, knockdown of SNHG4 could repress the neuroinflammation via inhibiting IL-6, IL-12, and TNF-α while inducing IL-10 levels. Additionally, miR-423-5p was predicted as the target of SNHG4 by employing bioinformatics analysis. miR-423-5p has been reported to exert significantly poorer in several diseases. However, the role of miR-423-5p in the development of neuropathic pain is needed to be clarified. Here, in our investigation, RIP assay confirmed the correlation between miR-423-5p and SNHG4. Meanwhile, we found that miR-423-5p was significantly decreased in SNL rat models. SNHG4 regulated miR-423-5p expression negatively. As exhibited, the loss of miR-423-5p contributed to neuropathic pain progression, which was rescued by the silence of SNHG4. Therefore, our study indicated SNHG4 as a novel therapeutic target for neuropathic pain via sponging miR-423-5p.

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Section: Discussionmentioning

confidence: 99%

Loss of SNHG4 Attenuated Spinal Nerve Ligation-Triggered Neuropathic Pain through Sponging miR-423-5p

Pan

Shen

Huang

et al. 2020

Mediators of Inflammation

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“…A significant reduction in miR-142-3p expression was observed in DRG of mice with SNL. Overexpression of miR-142-3p inhibited neuropathic pain and neuroinflammation through targeting high mobility group box 1 (HMGB1)(Zhang et al, 2018 ). This indicated that miR-142-3p may serve as a potential therapeutic target for neuropathic pain.…”

Section: Regulatory Mechanisms Of Micrornas In Chronic Painmentioning

confidence: 99%

The Regulatory Mechanisms and Therapeutic Potential of MicroRNAs: From Chronic Pain to Morphine Tolerance

Dai

et al. 2018

Front. Mol. Neurosci.

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Chronic pain, including cancer-related pain, is a pain condition often caused by inflammation or dysfunctional nerves. Chronic pain treatment poses a significant health care challenge, where opioids especially morphine are widely used and patients often develop tolerance over time with aggravated pain. microRNA (miRNA) is known to play important roles in regulating gene expressions in the nervous system to affect neuronal network plasticity related to algogenesis and the developing of morphine tolerance. In this article, we reviewed studies conducted in rodent animal models investigating the mechanisms of miRNAs regulation in chronic pain with different phenotypes and morphine tolerance. In addition, the potential of targeting miRNAs for chronic pain and morphine tolerance treatment is also reviewed. Finally, we point out the directions of the future research in chronic pain and morphine tolerance.

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“…In this study, we demonstrated that BDNF expression is regulated by miR-142-3p, the highly upregulated miRNA upon microglial activation, through its target CAMK2A. Several studies have shown that miR-142-3p functions as a regulator of neuroinflammation by modulating the expression of proinflammatory mediators in response to different pathological stimuli, such as multiple sclerosis, neuropathic pain, human immunodeficiency virus (HIV) and simian immunodeficiency virus encephalitis (SIVE; Chaudhuri et al, 2013;Talebi et al, 2017;Zhang et al, 2018). This study reveals a novel role of miR-142-3p in activated microglia as its upregulation upon microglial activation perturbs the CAMK2A-CREB-BDNF signaling pathway, which is involved in synaptic plasticity.…”

Section: Discussionmentioning

confidence: 89%

miR-142-3p Regulates BDNF Expression in Activated Rodent Microglia Through Its Target CAMK2A

Gupta

Jadhav

Tan

et al. 2020

Front. Cell. Neurosci.

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Microglia, the innate immune effector cells of the mammalian central nervous system (CNS), are involved in the development, homeostasis, and pathology of CNS. Microglia become activated in response to various insults and injuries and protect the CNS by phagocytosing the invading pathogens, dead neurons, and other cellular debris. Recent studies have demonstrated that the epigenetic mechanisms ensure the coordinated regulation of genes involved in microglial activation. In this study, we performed a microRNA (miRNA) microarray in activated primary microglia derived from rat pup's brain and identified differentially expressed miRNAs targeting key genes involved in cell survival, apoptosis, and inflammatory responses. Interestingly, miR-142-3p, one of the highly up-regulated miRNAs in microglia upon lipopolysaccharide (LPS)-mediated activation, compared to untreated primary microglia cells was predicted to target Ca 2+ /calmodulin dependent kinase 2a (CAMK2A). Further, luciferase reporter assay confirmed that miR-142-3p targets the 3 UTR of Camk2a. CAMK2A has been implicated in regulating the expression of brain-derived neurotrophic factor (BDNF) and long-term potentiation (LTP), a cellular mechanism underlying memory and learning. Given this, this study further focused on understanding the miR-142-3p mediated regulation of the CAMK2A-BDNF pathway via Cyclic AMP-responsive element-binding protein (CREB) in activated microglia. The results revealed that CAMK2A was downregulated in activated microglia, suggesting an inverse relationship between miR-142-3p and Camk2a in activated microglia. Overexpression of miR-142-3p in microglia was found to decrease the expression of CAMK2A and subsequently BDNF through regulation of CREB phosphorylation. Functional analysis through shRNA-mediated stable knockdown of CAMK2A in microglia confirmed that the regulation of BDNF by miR-142-3p is via CAMK2A. Overall, this study provides a database of differentially expressed miRNAs in activated primary microglia and reveals that microglial miR-142-3p regulates the CAMK2A-CREB-BDNF pathway which is involved in synaptic plasticity.

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MicroRNA-142-3p relieves neuropathic pain by targeting high mobility group box 1

Cited by 24 publications

References 64 publications

Loss of SNHG4 Attenuated Spinal Nerve Ligation-Triggered Neuropathic Pain through Sponging miR-423-5p

Loss of SNHG4 Attenuated Spinal Nerve Ligation-Triggered Neuropathic Pain through Sponging miR-423-5p

The Regulatory Mechanisms and Therapeutic Potential of MicroRNAs: From Chronic Pain to Morphine Tolerance

miR-142-3p Regulates BDNF Expression in Activated Rodent Microglia Through Its Target CAMK2A

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