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

Yan, Xuetao; Zhao, Ying; Cheng, Xiaoli; He, Xiang-Hu; Wang, Yu; Zheng, Wenzhong; Hu, Changwei; Wang, Yanlin

doi:10.1002/jcp.26284

Cited by 35 publications

(36 citation statements)

References 43 publications

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“…XIST can accelerate neuropathic pain progression through the regulation of miR‐150 and ZEB1 in CCI rat models. miR‐200b/miR‐429 can participate in neuropathic pain development by targeting Zeb1 . In our current study, we observed that Zeb1 was elevated in CCI rats.…”

Section: Discussionsupporting

confidence: 55%

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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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Section: Discussionsupporting

confidence: 55%

“…33 I n addition, recently, Zeb1 has been reported to be involved in neuropathic pain development. 34,35 XIST can accelerate neuropathic pain progression through the regulation of miR-150 and ZEB1 in CCI rat models. miR-200b/miR-429 can participate in neuropathic pain development by targeting Zeb1.…”

Section: Discussionmentioning

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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“…MiR‐155 can regulate inflammation response through SOCS1–STAT3–PDCD4 in atherogenesis (Ye et al, ). LncRNA MEG3 can regulate ischemic neuronal death via targeting miR‐21/PDCD4 (H. Yan, Rao et al, ; X. T. Yan, Zhao et al, ). MiR‐499 can protect endothelial cells against inflammatory damage by inhibiting NF‐κB/TNF‐α by targeting PDCD4 in coronary artery disease (Y. H. Zhang, He, & Shi, ).…”

Section: Discussionmentioning

confidence: 99%

DGCR5 attenuates neuropathic pain through sponging miR‐330‐3p and regulating PDCD4 in CCI rat models

Peng

Zhang

et al. 2018

Journal Cellular Physiology

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Neuropathic pain caused by somatosensory nervous system dysfunction is a serious public health problem. Some long noncoding RNAs (lncRNAs) can participate in physiological processes involved in neuropathic pain. However, the effects of lncRNA DGCR5 in neuropathic pain have not been explored. Therefore, in our current study, we concentrated on the biological roles of DGCR5 in neuropathic pain. Here, it was observed that DGCR5 was significantly decreased in chronic sciatic nerve injury (CCI) rat models. DGCR5 overexpression was able to alleviate neuropathic pain development including mechanical and thermal hyperalgesia. In addition, the current understanding of miR-330-3p function in neuropathic pain remains largely incomplete. Here, we found that miR-330-3p was greatly increased in CCI rats and DGCR5 can modulate miR-330-3p expression negatively. Upregulation of DGCR5 repressed inflammation-correlated biomarkers including interleukin 6 (IL-6), tumor necrosis factor α, and IL-1β in CCI rats by sponging miR-330-3p. The negative correlation between DGCR5 and miR-330-3pwas confirmed in our current study. Inhibition of miR-330-3p suppressed neuropathic pain progression by restraining neuroinflammation in vivo. In addition, PDCD4 was predicted as a downstream target of miR-330-3p. Furthermore, PDCD4 was significantly increased in CCI rats and DGCR5 regulated PDCD4 expression through sponging miR-330-3p in CCI rat models. Taken these together, it was implied that DGCR5/miR-330-3p/PDCD4 axis participated in neuropathic pain treatment. K E Y W O R D SDGCR5, miR-330-3p, neuropathic pain, PDCD4

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“…At the same time several miRNAs, such as miR-200b and miR-429, are down-regulated in microglia after nerve injury, and Zeb1 (Zinc finger E-box binding homeobox 1) has been identified as a target of these two miRNAs [109]. Zeb family members are essential for the developing nociceptors in the DRG [138].…”

Section: Mirnas Deregulated In the Peripheral Nervementioning

confidence: 99%

Non-coding RNAs in neuropathic pain

2020

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Neuro-immune alterations in the peripheral and central nervous system play a role in the pathophysiology of chronic pain in general, and members of the non-coding RNA (ncRNA) family, specifically the short, 22 nucleotide microRNAs (miRNAs) and the long non-coding RNAs (lncRNAs) act as master switches orchestrating both immune as well as neuronal processes. Several chronic disorders reveal unique ncRNA expression signatures, which recently generated big hopes for new perspectives for the development of diagnostic applications. lncRNAs may offer perspectives as candidates indicative of neuropathic pain in liquid biopsies. Numerous studies have provided novel mechanistic insight into the role of miRNAs in the molecular sequelae involved in the pathogenesis of neuropathic pain along the entire pain pathway. Specific processes within neurons, immune cells, and glia as the cellular components of the neuropathic pain triad and the communication paths between them are controlled by specific miRNAs. Therefore, nucleotide sequences mimicking or antagonizing miRNA actions can provide novel therapeutic strategies for pain treatment, provided their human homologues serve the same or similar functions. Increasing evidence also sheds light on the function of lncRNAs, which converge so far mainly on purinergic signalling pathways both in neurons and glia, and possibly even other ncRNA species that have not been explored so far.

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

Cited by 35 publications

References 43 publications

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

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

DGCR5 attenuates neuropathic pain through sponging miR‐330‐3p and regulating PDCD4 in CCI rat models

Non-coding RNAs in neuropathic pain

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