The role of miR-190a-5p contributes to diabetic neuropathic pain via targeting SLC17A6

Yang, Di; Yang, Qinyan; Wei, Xin; Liu, Yang; Ma, Ding; Li, Jiaceng; Wan, Yongling; Luo, Yong

doi:10.2147/jpr.s133755

Cited by 48 publications

(47 citation statements)

References 35 publications

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“…This is consistent with previous studies, 26 which demonstrated that the production and release of various inflammatory cytokines and chemo-kines, such as TNF-α, IL-1β and IL-6, are rapidly increased within 1–3 days after spinal nerve injury. 27 – 30 In our study, the symptoms of mechanical allodynia and thermal hyperalgesia appeared to be most prominent, 19 as well as the expression of inflammatory cytokines and chemokines on day 3 following nerve injury. All the studied cytokines play a major role in pain processing and regional, intrathecal or intracerebro-ventricular injection of IL-1β or/and IL-6 has been found to induce dramatic pain hypersensitivity in rats and mice.…”

Section: Discussionsupporting

confidence: 45%

Pro-resolving mediator maresin 1 ameliorates pain hypersensitivity in a rat spinal nerve ligation model of neuropathic pain

Gao¹,

Tang²,

Tai³

et al. 2018

JPR

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BackgroundPro-resolving mediators (PRMs) are considered as emerging analgesics for chronic pain. Maresin 1 (MaR1) is a newly identified member of PRMs, and recent studies implicate its potential role in some pain conditions. As the function of MaR1 in neuropathic pain remains unclear, we investigated the effects of MaR1 on pain hypersensitivity and the underlying mechanism using a rat spinal nerve ligation (SNL) model of neuropathic pain.Materials and methodsMaR1 (100 ng/10 μL) or commensurable artificial cerebrospinal fluid was delivered via intrathecal catheter from days 3 to 5 post-SNL followed by assessment of mechanical allodynia and thermal hyperalgesia. Ipsilateral L4–L5 spinal cord tissue was collected on day 7 post-SNL and assessed by Western blotting, enzyme-linked immunosorbent assay or immunohistochemistry.ResultsIntrathecal MaR1 significantly attenuated mechanical allodynia and thermal hyperalgesia from day 5 to day 7 post-SNL, which was associated with decreased spinal levels of glial markers, GFAP and IBA1. It was also found that intrathecal MaR1 downregulated phosphorylation levels of NF-κB p65 and its nuclear translocation, as well as decreased protein levels of pro-inflammatory cytokines, TNF-α, IL-1β and IL-6. Further, MaR1 treatment restored PSD95 and synapsin II levels, suggesting that MarR1 also protected synaptic integrity.ConclusionOur results indicate that MaR1 ameliorates the SNL-induced neuropathic pain by regulating glial activities and pro-inflammatory cytokines release. The present study offers insight into the potential of MaR1 as a novel intervention to ameliorate neuropathic pain.

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Section: Discussionsupporting

confidence: 45%

Pro-resolving mediator maresin 1 ameliorates pain hypersensitivity in a rat spinal nerve ligation model of neuropathic pain

Gao¹,

Tang²,

Tai³

et al. 2018

JPR

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“…miR‐183 can inhibit neuropathic pain by targeting mammalian target of rapamycin (mTOR)/vascular endothelial growth factor (VEGF) pathway . The downregulation of miR‐128 leads to neuropathic pain by activating P38 . MiR‐155 can modulate neuropathic pain progression by targeting SGK3 .…”

Section: Introductionmentioning

confidence: 99%

MiR‐28‐5p relieves neuropathic pain by targeting Zeb1 in CCI rat models

Bao

Wang

Xie

et al. 2018

J of Cellular Biochemistry

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MicroRNAs (miRNAs) are recognized as significant regulators of neuropathic pain. Moreover, neuroinflammation can contribute a lot to the progression of neuropathic pain. MiR-28-5p has been reported to be involved in many pathological diseases. However, little is known about the function of miR-28-5p in neuropathic pain development. Our current study was designed to investigate the biological roles of miR-28-5p in neuropathic pain in a rat model established by chronic sciatic nerve injury (CCI). Here, we observed that miR-28-5p was decreased in CCI rats. MiR-28-5p overexpression was able to alleviate neuropathic pain behaviors including mechanical and thermal hyperalgesia. Meanwhile, inflammation-correlated biomarkers such as Cyclooxygenase 2 (Cox-2), interleukin-6 (IL-6), and IL-1β were greatly promoted in CCI rats and they were inhibited by miR-28-5p upregulation. In addition, zinc finger E-box-binding homeobox 1 (Zeb1) is a kind of transcription factor that is involved in various diseases. Here, in our study, Zeb1 was predicted as a downstream target of miR-28-5p. miR-28-5p can bind with the 3'-untranslated region of Zeb1, which was validated by carrying out dual-luciferase reporter assay. Moreover, we found that Zeb1 was significantly increased in CCI rats and miR-28-5p can modulate Zeb1 expression negatively. Theoverexpression of Zeb1 can disturb neuropathic pain development, which was repressed by the increase of miR-28-5p by upregulating Cox-2, IL-6, and IL-1β levels. By taking all of these together, it was indicated in our study that miR-28-5p can reduce neuropathic pain progression by targeting Zeb1 in vivo. Our data implied that miR-28-5p/Zeb1 axis can be a novel therapeutic target for neuropathic pain treatment.

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“…Based on the current literature and our own in vitro data showing spine loss after treatment with BDEs, it could be hypothesized that downregulation of let-7c in the BDEs could possibly lead to increased inflammation, resulting in neuronal impairment and synapse dysfunction in the PNO offspring during synaptogenesis. On these lines, miR-190a-5p downregulation in the spinal cord has been associated with diabetic neuropathic pain in a rat model [78]. The authors provide evidence that miR-190a-5p downregulation causes an increase in the expression of its target, vesicular glutamate transporter 2 (vGLUT2), and induces the expression of the inflammatory cytokines IL-6 and IL-1β.…”

Section: Discussionmentioning

confidence: 96%

Brain-Derived Extracellular Vesicle microRNA Signatures Associated with In Utero and Postnatal Oxycodone Exposure

Shahjin

Guda

Schaal

et al. 2019

Cells

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Oxycodone (oxy) is a semi-synthetic opioid commonly used as a pain medication that is also a widely abused prescription drug. While very limited studies have examined the effect of in utero oxy (IUO) exposure on neurodevelopment, a significant gap in knowledge is the effect of IUO compared with postnatal oxy (PNO) exposure on synaptogenesis-a key process in the formation of synapses during brain development-in the exposed offspring. One relatively unexplored form of cell-cell communication associated with brain development in response to IUO and PNO exposure are extracellular vesicles (EVs). EVs are membrane-bound vesicles that serve as carriers of cargo, such as microRNAs (miRNAs). Using RNA-Seq analysis, we identified distinct brain-derived extracellular vesicle (BDEs) miRNA signatures associated with IUO and PNO exposure, including their gene targets, regulating key functional pathways associated with brain development to be more impacted in the IUO offspring. Further treatment of primary 14-day in vitro (DIV) neurons with IUO BDEs caused a significant reduction in spine density compared to treatment with BDEs from PNO and saline groups. In summary, our studies identified for the first time, key BDE miRNA signatures in IUO-and PNO-exposed offspring, which could impact their brain development as well as synaptic function.Cells 2020, 9, 21 2 of 18 lack of studies that have compared the effect of in utero oxy (IUO) and postnatal oxy (PNO) exposure on synaptogenesis-a key process of the formation of synapses during brain development-in the exposed offspring. Synapses are key communication points between neurons, which play a critical role in the regulation of neurotransmission and brain plasticity [6].One relatively unexplored form of cell-cell communication associated with brain development in response to IUO and PNO exposure is extracellular vesicles (EVs) [7][8][9]. These membrane-bound vesicles, comprised of exosomes and microvesicles, originate from the multivesicular bodies and plasma membrane, respectively. Furthermore, these EVs, which carry a repertoire of cargo, including microRNAs (miRNAs), are shown to induce inflammation and subsequent neuronal damage, thus serving as key mediators of pathogenesis in several neurological and neurodegenerative disorders [10,11]. The main objective of this study was to identify differentially expressed BDEs miRNAs using RNA sequencing (RNA-Seq) and evaluate their impact on synaptic architecture during a key stage of brain development.

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The role of miR-190a-5p contributes to diabetic neuropathic pain via targeting SLC17A6

Cited by 48 publications

References 35 publications

Pro-resolving mediator maresin 1 ameliorates pain hypersensitivity in a rat spinal nerve ligation model of neuropathic pain

Pro-resolving mediator maresin 1 ameliorates pain hypersensitivity in a rat spinal nerve ligation model of neuropathic pain

MiR‐28‐5p relieves neuropathic pain by targeting Zeb1 in CCI rat models

Brain-Derived Extracellular Vesicle microRNA Signatures Associated with In Utero and Postnatal Oxycodone Exposure

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