miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain
Background. miRNA is an essential factor in neuropathic pain. However, the underlying mechanism of miRNA in neuropathic pain remains unclear. Objective. To explore the potential role of miR-223 in neuropathic pain in a mice model of chronic sciatic nerve injury. Methods. Mice were divided into the s...
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Language: | English |
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Wiley
2021-01-01
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Series: | Pain Research and Management |
Online Access: | http://dx.doi.org/10.1155/2021/6674028 |
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author | Junsong Zhu Jinmei Yang Jianguo Xu |
author_facet | Junsong Zhu Jinmei Yang Jianguo Xu |
author_sort | Junsong Zhu |
collection | DOAJ |
description | Background. miRNA is an essential factor in neuropathic pain. However, the underlying mechanism of miRNA in neuropathic pain remains unclear. Objective. To explore the potential role of miR-223 in neuropathic pain in a mice model of chronic sciatic nerve injury. Methods. Mice were divided into the sham group, CCI group, CCI + Lenti-vector group, and CCI + Lenti-miR-223 group. Flow cytometry was used to detect the neuronal apoptosis and the proportion of M1/M2 macrophages in each group. Western blot was used to detect the protein expression levels of ASC, caspase-1, IL-1β, and IL-18 in each group. Luciferase activity assay detects the binding of miR-223 and NLRP3. Macrophage chemotaxis experiments verified the anti-inflammatory effect of miR-223 in vitro. Results. The overexpression of miR-233 significantly reduced the neuropathic pain caused by CCI and reduced the apoptosis and inflammatory factor expression. miR-223 inhibits the expression of NLRP3 by directly binding to the 3′-untranslated region. Overexpression of miR-223 reduces the protein levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the spinal cord of CCI mice, increases the proportion of M2-type macrophages, and reduces the proportion of M1-type macrophages. Conclusion. miR-223 may facilitate the development of neuropathic pain in CCI mice by inhibiting NLRP3-mediated neuroinflammation. |
format | Article |
id | doaj-art-14ccb43f003a40b397b621e6c5a74b70 |
institution | Kabale University |
issn | 1203-6765 1918-1523 |
language | English |
publishDate | 2021-01-01 |
publisher | Wiley |
record_format | Article |
series | Pain Research and Management |
spelling | doaj-art-14ccb43f003a40b397b621e6c5a74b702025-02-03T06:10:47ZengWileyPain Research and Management1203-67651918-15232021-01-01202110.1155/2021/66740286674028miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic PainJunsong Zhu0Jinmei Yang1Jianguo Xu2Pain Department, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan 430081, ChinaWuhan Hospital of Traditional Chinese and Western Medicine, Wuhan 430022, ChinaHubei Provincial Hospital of Traditional Chinese Medicine, Wuhan 430061, ChinaBackground. miRNA is an essential factor in neuropathic pain. However, the underlying mechanism of miRNA in neuropathic pain remains unclear. Objective. To explore the potential role of miR-223 in neuropathic pain in a mice model of chronic sciatic nerve injury. Methods. Mice were divided into the sham group, CCI group, CCI + Lenti-vector group, and CCI + Lenti-miR-223 group. Flow cytometry was used to detect the neuronal apoptosis and the proportion of M1/M2 macrophages in each group. Western blot was used to detect the protein expression levels of ASC, caspase-1, IL-1β, and IL-18 in each group. Luciferase activity assay detects the binding of miR-223 and NLRP3. Macrophage chemotaxis experiments verified the anti-inflammatory effect of miR-223 in vitro. Results. The overexpression of miR-233 significantly reduced the neuropathic pain caused by CCI and reduced the apoptosis and inflammatory factor expression. miR-223 inhibits the expression of NLRP3 by directly binding to the 3′-untranslated region. Overexpression of miR-223 reduces the protein levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the spinal cord of CCI mice, increases the proportion of M2-type macrophages, and reduces the proportion of M1-type macrophages. Conclusion. miR-223 may facilitate the development of neuropathic pain in CCI mice by inhibiting NLRP3-mediated neuroinflammation.http://dx.doi.org/10.1155/2021/6674028 |
spellingShingle | Junsong Zhu Jinmei Yang Jianguo Xu miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain Pain Research and Management |
title | miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain |
title_full | miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain |
title_fullStr | miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain |
title_full_unstemmed | miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain |
title_short | miR-223 Inhibits the Polarization and Recruitment of Macrophages via NLRP3/IL-1β Pathway to Meliorate Neuropathic Pain |
title_sort | mir 223 inhibits the polarization and recruitment of macrophages via nlrp3 il 1β pathway to meliorate neuropathic pain |
url | http://dx.doi.org/10.1155/2021/6674028 |
work_keys_str_mv | AT junsongzhu mir223inhibitsthepolarizationandrecruitmentofmacrophagesvianlrp3il1bpathwaytomeliorateneuropathicpain AT jinmeiyang mir223inhibitsthepolarizationandrecruitmentofmacrophagesvianlrp3il1bpathwaytomeliorateneuropathicpain AT jianguoxu mir223inhibitsthepolarizationandrecruitmentofmacrophagesvianlrp3il1bpathwaytomeliorateneuropathicpain |