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MicroRNA-128-3p Alleviates Neuropathic Pain Through Targeting ZEB1
Xianlong Zhang1, Yang Zhang1, Wei Cai2
1Department of Anesthesiology, The Affiliated Huai'an NO.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, China.
Abstract:
Neuropathic pain is defined as a chronic pain. It could be resulted from a lesion of nervous systems. MicroRNAs have been reported to modulate multiple genes and pathways in neuropathic pain and neuroinflammation. Therefore, identifying the potential expression patterns of microRNAs under neuropathic pain conditions is significant. miR-128-3p has been identified in many cancers. But, its biological role in neuropathic pain progression remains poorly known. Currently, we aimed to explore the possible functions of miR-128-3p in the modulation of neuropathic pain. We displayed in the CCI rats, miR-128-3p was greatly down-regulated in the spinal cord tissues and the isolated microglias. Subsequently, LV-miR-128-3p could attenuate CCI-triggered mechanical allodynia and thermal hyperalgesia. Meanwhile, some common pro-inflammatory cytokines were significantly reduced while anti-inflammatory cytokine IL-10 was increased by miR-128-3p. Here, in the current investigation, by utilizing dual-luciferase reporter assays, ZEB1 was proved as a direct target of miR-128-3p. LV-miR-128-3p significantly repressed ZEB1 expression in microglia of CCI rats. Moreover, ZEB1 was reported to be increased in CCI rats. miR-128-3p rescued the effects of ZEB1 on neuropathic pain progression via inhibiting neuroinflammation. Taken these together, we implied miR-128-3p alleviated the progression of neuropathic pain via modulating ZEB1.
Insights
MicroRNA-128-3p (miR-128-3p) is down-regulated in neuropathic pain. Restoring miR-128-3p levels alleviates pain and neuroinflammation by targeting ZEB1.
Area of Science:
- Neuroscience
- Molecular Biology
- Pain Research
Background:
- Neuropathic pain arises from nervous system lesions and involves complex molecular pathways.
- MicroRNAs (miRNAs) are key regulators of gene expression implicated in neuropathic pain and neuroinflammation.
- The specific role of miR-128-3p in neuropathic pain remains largely unexplored, despite its known involvement in cancers.
Purpose of the Study:
- To investigate the function and regulatory mechanisms of miR-128-3p in the context of neuropathic pain.
- To determine if miR-128-3p expression is altered in neuropathic pain models.
- To explore the therapeutic potential of modulating miR-128-3p in alleviating neuropathic pain symptoms.
Main Methods:
- Establishment of a chronic constriction injury (CCI) rat model to induce neuropathic pain.
- Quantification of miR-128-3p expression in spinal cord tissues and isolated microglia from CCI rats.
- In vivo delivery of miR-128-3p using lentiviral vectors (LV-miR-128-3p) to assess its therapeutic effects.
- Measurement of pain behaviors (mechanical allodynia, thermal hyperalgesia) and inflammatory cytokine levels (pro- and anti-inflammatory).
- Dual-luciferase reporter assays to identify and validate ZEB1 as a direct target of miR-128-3p.
- Assessment of ZEB1 expression in microglia of CCI rats and its modulation by miR-128-3p.
Main Results:
- miR-128-3p was significantly downregulated in the spinal cord and microglia of CCI rats.
- Overexpression of miR-128-3p using LV-miR-128-3p attenuated mechanical allodynia and thermal hyperalgesia in CCI rats.
- miR-128-3p treatment reduced pro-inflammatory cytokines and increased the anti-inflammatory cytokine IL-10.
- ZEB1 was confirmed as a direct target of miR-128-3p and its expression was elevated in CCI rats.
- LV-miR-128-3p inhibited ZEB1 expression in microglia and mitigated ZEB1-induced effects on neuropathic pain progression and neuroinflammation.
Conclusions:
- miR-128-3p plays a protective role in neuropathic pain by suppressing neuroinflammation.
- The therapeutic effect of miR-128-3p involves the direct inhibition of ZEB1 expression.
- Modulating miR-128-3p represents a potential therapeutic strategy for managing neuropathic pain.
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