MiR-150 alleviates neuropathic pain via inhibiting toll-like receptor 5

Li-Juan Ji; Jing Shi; Jing-Min Lu; Qiang-min Huang

doi:10.1002/jcb.26269

MiR-150 alleviates neuropathic pain via inhibiting toll-like receptor 5

Journal of Cellular Biochemistry ◽

10.1002/jcb.26269 ◽

2017 ◽

Vol 119 (1) ◽

pp. 1017-1026 ◽

Cited By ~ 27

Author(s):

Li-Juan Ji ◽

Jing Shi ◽

Jing-Min Lu ◽

Qiang-min Huang

Keyword(s):

Neuropathic Pain ◽

Toll Like Receptor ◽

Toll Like Receptor 5

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LncRNA X inactive specific transcript contributes to neuropathic pain development by sponging miR‐154‐5p via inducing toll‐like receptor 5 in CCI rat models

Journal of Cellular Biochemistry ◽

10.1002/jcb.27088 ◽

2018 ◽

Vol 120 (2) ◽

pp. 1271-1281 ◽

Cited By ~ 10

Author(s):

Meng Wei ◽

Lin Li ◽

Yang Zhang ◽

Zhi‐Jie Zhang ◽

Hai‐Lin Liu ◽

...

Keyword(s):

Neuropathic Pain ◽

Toll Like Receptor ◽

Rat Models ◽

Specific Transcript ◽

Toll Like Receptor 5

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Cross-Talk of Toll-Like Receptor 5 and Mu-Opioid Receptor Attenuates Chronic Constriction Injury-Induced Mechanical Hyperalgesia through a Protein Kinase C Alpha-Dependent Signaling

International Journal of Molecular Sciences ◽

10.3390/ijms22041891 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1891

Author(s):

Ching Chang ◽

Hung-Kai Liu ◽

Chao-Bin Yeh ◽

Ming-Lin Yang ◽

Wen-Chieh Liao ◽

...

Keyword(s):

Neuropathic Pain ◽

Protein Kinase ◽

Chronic Constriction Injury ◽

Intrathecal Administration ◽

Mu Opioid Receptor ◽

Mechanical Hyperalgesia ◽

Toll Like Receptor ◽

Mu Opioid ◽

Kinase C ◽

Toll Like Receptor 5

Recently, Toll-like receptors (TLRs), a family of pattern recognition receptors, are reported as potential modulators for neuropathic pain; however, the desired mechanism is still unexplained. Here, we operated on the sciatic nerve to establish a pre-clinical rodent model of chronic constriction injury (CCI) in Sprague-Dawley rats, which were assigned into CCI and Decompression groups randomly. In Decompression group, the rats were performed with nerve decompression at post-operative week 4. Mechanical hyperalgesia and mechanical allodynia were obviously attenuated after a month. Toll-like receptor 5 (TLR5)-immunoreactive (ir) expression increased in dorsal horn, particularly in the inner part of lamina II. Additionally, substance P (SP) and isolectin B4 (IB4)-ir expressions, rather than calcitonin-gene-related peptide (CGRP)-ir expression, increased in their distinct laminae. Double immunofluorescence proved that increased TLR5-ir expression was co-expressed mainly with IB4-ir expression. Through an intrathecal administration with FLA-ST Ultrapure (a TLR5 agonist, purified flagellin from Salmonella Typhimurium, only the CCI-induced mechanical hyperalgesia was attenuated dose-dependently. Moreover, we confirmed that mu-opioid receptor (MOR) and phospho-protein kinase Cα (pPKCα)-ir expressions but not phospho-protein kinase A RII (pPKA RII)-ir expression, increased in lamina II, where they mostly co-expressed with IB4-ir expression. Go 6976, a potent protein kinase C inhibitor, effectively reversed the FLA-ST Ultrapure- or DAMGO-mediated attenuated trend towards mechanical hyperalgesia by an intrathecal administration in CCI rats. In summary, our current findings suggest that nerve decompression improves CCI-induced mechanical hyperalgesia that might be through the cross-talk of TLR5 and MOR in a PKCα-dependent manner, which opens a novel opportunity for the development of analgesic therapeutics in neuropathic pain.

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