Weiwei Zheng , Peng Zhang , Hui Che , Yu Zhang , Xing Yang , Yixin Shen
{"title":"GsMTx4通过Piezo1/NFκB/STAT6途径调节小胶质细胞极化，从而改善脊髓损伤","authors":"Weiwei Zheng , Peng Zhang , Hui Che , Yu Zhang , Xing Yang , Yixin Shen","doi":"10.1016/j.jnrt.2024.100144","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><p>Inflammatory reactions are recognized as pivotal in spinal cord injury (SCI), with the anti-inflammatory role of polarized microglia crucial in mitigating such injury. The present study aimed to determine the protective effects of GsMTx4 on functional recovery in a mouse model of SCI and investigate the role of GsMTx4 in cytokine-induced microglial activation and associated molecular mechanisms.</p></div><div><h3>Methods</h3><p>We assessed the effects of GsMTx4 on motor function in a mouse model of SCI, including neuronal survival and activated microglia in the vicinity of the injury after SCI. We also investigated the effects of GsMTx4 on expression of relevant inflammatory factors involved in cytokine-induced microglial activation and the associated signaling pathways.</p></div><div><h3>Results</h3><p>GsMTx4 effectively promoted functional recovery in mice and alleviated nerve damage after SCI. Additionally, GsMTx4 facilitated the transition of microglia from the M1 phenotype to the M2 phenotype, suppressed microglial activation, and reduced the expression of corresponding inflammatory mediators. These effects may involve modulation of neurogenic inflammation through the Piezo1/NFκB/STAT6 pathway, at least in part.</p></div><div><h3>Conclusion</h3><p>GsMTx4 safeguards against SCI by regulating microglial polarization, potentially via the Piezo1/NFκB/STAT6 pathway, offering initial evidence supporting the potential therapeutic efficacy of GsMTx4 for treatment of SCI.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 4","pages":"Article 100144"},"PeriodicalIF":3.1000,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000512/pdfft?md5=bfe78d8fe1add4d4db5e0233b5e29251&pid=1-s2.0-S2324242624000512-main.pdf","citationCount":"0","resultStr":"{\"title\":\"GsMTx4 ameliorates spinal cord injury by regulating microglial polarization through the Piezo1/NFκB/STAT6 pathway\",\"authors\":\"Weiwei Zheng , Peng Zhang , Hui Che , Yu Zhang , Xing Yang , Yixin Shen\",\"doi\":\"10.1016/j.jnrt.2024.100144\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Objective</h3><p>Inflammatory reactions are recognized as pivotal in spinal cord injury (SCI), with the anti-inflammatory role of polarized microglia crucial in mitigating such injury. The present study aimed to determine the protective effects of GsMTx4 on functional recovery in a mouse model of SCI and investigate the role of GsMTx4 in cytokine-induced microglial activation and associated molecular mechanisms.</p></div><div><h3>Methods</h3><p>We assessed the effects of GsMTx4 on motor function in a mouse model of SCI, including neuronal survival and activated microglia in the vicinity of the injury after SCI. We also investigated the effects of GsMTx4 on expression of relevant inflammatory factors involved in cytokine-induced microglial activation and the associated signaling pathways.</p></div><div><h3>Results</h3><p>GsMTx4 effectively promoted functional recovery in mice and alleviated nerve damage after SCI. Additionally, GsMTx4 facilitated the transition of microglia from the M1 phenotype to the M2 phenotype, suppressed microglial activation, and reduced the expression of corresponding inflammatory mediators. These effects may involve modulation of neurogenic inflammation through the Piezo1/NFκB/STAT6 pathway, at least in part.</p></div><div><h3>Conclusion</h3><p>GsMTx4 safeguards against SCI by regulating microglial polarization, potentially via the Piezo1/NFκB/STAT6 pathway, offering initial evidence supporting the potential therapeutic efficacy of GsMTx4 for treatment of SCI.</p></div>\",\"PeriodicalId\":44709,\"journal\":{\"name\":\"Journal of Neurorestoratology\",\"volume\":\"12 4\",\"pages\":\"Article 100144\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2024-08-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S2324242624000512/pdfft?md5=bfe78d8fe1add4d4db5e0233b5e29251&pid=1-s2.0-S2324242624000512-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Neurorestoratology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2324242624000512\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Neurorestoratology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2324242624000512","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
GsMTx4 ameliorates spinal cord injury by regulating microglial polarization through the Piezo1/NFκB/STAT6 pathway
Objective
Inflammatory reactions are recognized as pivotal in spinal cord injury (SCI), with the anti-inflammatory role of polarized microglia crucial in mitigating such injury. The present study aimed to determine the protective effects of GsMTx4 on functional recovery in a mouse model of SCI and investigate the role of GsMTx4 in cytokine-induced microglial activation and associated molecular mechanisms.
Methods
We assessed the effects of GsMTx4 on motor function in a mouse model of SCI, including neuronal survival and activated microglia in the vicinity of the injury after SCI. We also investigated the effects of GsMTx4 on expression of relevant inflammatory factors involved in cytokine-induced microglial activation and the associated signaling pathways.
Results
GsMTx4 effectively promoted functional recovery in mice and alleviated nerve damage after SCI. Additionally, GsMTx4 facilitated the transition of microglia from the M1 phenotype to the M2 phenotype, suppressed microglial activation, and reduced the expression of corresponding inflammatory mediators. These effects may involve modulation of neurogenic inflammation through the Piezo1/NFκB/STAT6 pathway, at least in part.
Conclusion
GsMTx4 safeguards against SCI by regulating microglial polarization, potentially via the Piezo1/NFκB/STAT6 pathway, offering initial evidence supporting the potential therapeutic efficacy of GsMTx4 for treatment of SCI.
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