Effects of microRNA-223 on morphine analgesic tolerance by targeting <i>NLRP3</i> in a rat model of neuropathic pain

Xie, Xiaojuan; Ma, Ligang; Xi, Kai; Fan, Daiming; Li, Jianguo; Zhang, Quan; Zhang, Wei

doi:10.1177/1744806917706582

Cited by 39 publications

(23 citation statements)

References 41 publications

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“…Specifically, we demonstrated that the downregulation of miR-223 was closely associated with increased NLRP3 mRNA levels. This finding effectively supports the hypothesis that miR-223 acts as a negative regulator of NLRP3 inflammasome activity, as it was already observed in other pathological conditions (27,29). It is well recognized that NLRP3 is an important mediator involved in cell necroptosis (30), and it has been suggested that its activation may be modulated by Casp-8 (23,26).…”

Section: Discussionsupporting

confidence: 89%

“…These miRNAs have the ability to bind to their target Casp-8 mRNA transcript in order to facilitate the necroptosis of HCC cells. Additionally, the data presented herein confirm the well-known association between miR-223 and NLRP3, as already reported in different disease contexts (27)(28)(29)(30)(31).…”

Section: Introductionsupporting

confidence: 90%

“…Inverse association between miR-223 and NLRP3 in HCC samples. The miR-223-dependent post-transcriptional regulation of the NLRP3 inflammasome has been well validated in a variety of cell types (27,30); however, this functional link has not been established yet in HCC. Therefore, in this study, we proceeded to investigate whether an inverse correlation between miR-223 abundance and NLRP3 mRNA expression also exists in HCC.…”

Section: Mir-371-5p Mir-373 and Mir-543 Regulated Necroptosis Of Hccmentioning

confidence: 99%

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miRNA expression profiling regulates necroptotic cell death in hepatocellular carcinoma

et al. 2018

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Hepatocellular carcinoma (HCC) is one of the most aggressive types of cancer and is among the leading causes of cancer-related mortality worldwide. Although the dysregulation of microRNAs (miRNAs or miRs) has often been reported in HCC, the precise molecular mechanisms by which miRNAs modulate the process of tumorigenesis and the behavior of cancer cells are not yet clearly understood. In this study, we identified a novel three‑miRNA signature, including miR‑371-5p, miR‑373 and miR‑543, that appears to orchestrate programmed cell necrosis in HCC by directly targeting the caspase‑8 gene (Casp‑8). Our results demonstrated that miR‑371-5p, miR‑373 and miR‑543 were overexpressed in HCC tissues compared with paired adjacent normal tissues. The upregulation of these miRNAs specifically and markedly downregulated the expression of Casp‑8, as well as significantly enhanced the Z-VAD/TNF‑α-induced necroptosis of HCC cells. By contrast, the selective knockdown of miRNA expression led to a significant increase in Casp‑8 levels and a marked reduction in programmed cell necrosis. Intriguingly, the sustained overexpression of Casp‑8 reversed the pro‑necroptotic effects exerted by miRNA mimics. Finally, a strong inverse association between the level of miR‑223 and the expression levels of nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing-3 inflammasome was observed in our HCC specimens. On the whole, the present study revealed a molecular link between the three‑miRNA signature, comprising miR‑371-5p, miR‑373 and miR‑543, and the negative necroptotic regulator Casp‑8, and presents evidence for its employment as a novel potential diagnostic, prognostic and therapeutic target in HCC.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionsupporting

confidence: 90%

Section: Mir-371-5p Mir-373 and Mir-543 Regulated Necroptosis Of Hccmentioning

confidence: 99%

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miRNA expression profiling regulates necroptotic cell death in hepatocellular carcinoma

et al. 2018

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“…For instance, by regulating voltage‐gated potassium channels, miR‐17‐92 cluster can induce chronic neuropathic pain development (Sakai et al, ). miR‐223 could inactivate NLRP3 inflammasomes to relieve neuropathic pain (Xie et al, ). miR‐30b is able to attenuate neuropathic pain progression by targeting voltage‐gated sodium channel Nav1.3 in rat models (Su et al, ).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of miR‐200b/miR‐429 contributes to neuropathic pain development through targeting zinc finger E box binding protein‐1

Yan

Zhao

Cheng

et al. 2018

Journal Cellular Physiology

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Many studies have reported that microRNAs participate in neuropathic pain development. Previously, miR-200b and miR-429 are reported to be involved in various diseases. In our current study, we focused on their roles in neuropathic pain and we found that miR-200b and miR-429 were significantly decreased in chronic constriction injury (CCI) rat spinal cords and isolated microglials. miR-200b and miR-429 overexpression were able to relieve neuropathic pain through modulating PWT and PWL in CCI rats. Meanwhile, we observed that both miR-200b and miR-429 upregulation could repress neuroinflammation via inhibiting inflammatory cytokines such as IL-6, IL-1β, and TNF-α in CCI rats. By carry out bioinformatics technology, Zinc finger E box binding protein-1 (ZEB1) was predicted as target of miR-200b, and miR-429 and dual-luciferase reporter assays confirmed the correlation between them. ZEB1 has been reported to regulate a lot of diseases. Here, we found that ZEB1 was greatly increased in CCI rats and miR-200b and miR-429 overexpression markedly suppressed ZEB1 mRNA expression in rat microglial cells. In addition, knockdown of ZEB1 can reduce neuropathic pain development and co-transfection of LV-anti-miR-200b/miR-429 reversed this phenomenon in vivo. Taken these together, our results suggested that miR-200b/miR-429 can serve as an important regulator of neuropathic pain development by targeting ZEB1.

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“…Despite the absence of research on interaction between DEX and NLRP3, involvement of NLRP3 has been intensively investigated in research on neuropathic pain. For instance, microRNA-223 ameliorated morphine analgesic tolerance to neuropathic pain by down-regulating NLRP3 [21]. Paclitaxel activated neuropathic pain by stimulating NLRP3 in ammasome and pro-in ammatory factor IL-1β [22].…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine alleviates inflammation-induced neuropathic pain by suppressing NLRP3 via activation of Nrf2

Shan

Liao

Tang

et al. 2020

Preprint

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Objective: To investigate the mechanism of dexmedetomidine (DEX) involving Nrf2-dependent inhibition of NLRP3 in relieving neuropathic pain in chronic constriction injury (CCI) rat models.Methods: The CCI rat models were constructed through sciatic nerve ligation. The CCI rats were treated with DEX, Nrf2 inhibitor (ML385), NLRP3 antagonist (MCC950) and NLRP3 activator (Nigericin). Mechanical withdrawal threshold (MWT) was measured to test the pain sensitivity of CCI rats. H&E staining detected spinal injury of the rats and TUNEL staining was applied to test apoptosis in the spinal cords. ELISA measured the expressions of inflammatory factors. The expressions of Nrf2 and NLRP3 were also detected.Results: Decreased MWT, enhanced spinal cord injury, promoted apoptosis and increased inflammatory factors were detected in CCI rats. The expressions of the above indicators were retraced in DEX-treated CCI rats. Increased MWT, reduced spinal cord injury, inhibited apoptosis and decreased inflammatory factors were detected in rats treated with MCC950 or ML385 while opposite expression patterns were found in rats treated with Nigericin. The expressions of these indicators were retraced in both DEX+ML385 group and MCC950+ML385 group compared to ML385 group and MCC950 group respectively.Conclusion: DEX reduces neuropathic pain of CCI rats by suppressing NLRP3 through activation of Nrf2.

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Effects of microRNA-223 on morphine analgesic tolerance by targeting NLRP3 in a rat model of neuropathic pain

Cited by 39 publications

References 41 publications

miRNA expression profiling regulates necroptotic cell death in hepatocellular carcinoma

miRNA expression profiling regulates necroptotic cell death in hepatocellular carcinoma

Inhibition of miR‐200b/miR‐429 contributes to neuropathic pain development through targeting zinc finger E box binding protein‐1

Dexmedetomidine alleviates inflammation-induced neuropathic pain by suppressing NLRP3 via activation of Nrf2

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