{"title":"长非编码 RNA MALAT1 通过 miR-199a-5p/PRDM5 轴促进脊髓损伤过程中的神经细胞凋亡","authors":"Xieli Guo, Huan Chen, Suonan Li, Shuai Zhang, Yong Gong, Jiangliu Yin","doi":"10.5137/1019-5149.JTN.36175-21.5","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>To determine the regulation of long non-coding RNA (lncRNA) MALAT1 on neuronal apoptosis during spinal cord injury (SCI) and to explore its possible mechanisms.</p><p><strong>Material and methods: </strong>The motor ability of SCI rat models and apoptosis in spinal cord tissue were evaluated. Primary spinal cord neurons (SCNs) were isolated and treated with H2O2 before cell transfection. The apoptosis of SCNs and expression of PRDM5 and MALAT1 were also measured. The interactions among MALAT1, miR-199a-5p, and PRDM5 were detected.</p><p><strong>Results: </strong>The motor ability of SCI rats decreased significantly. The proportion of apoptotic neurons increased in damaged tissue and SCN, along with an increase in the expression of apoptosis-related proteins c-caspase-3/9, autophagy-related proteins (p62 and LC3 II/I ratio), and proinflammatory factors. Moreover, overexpression of MALAT1 and PRDM5 in damaged SCN resulted in an increased apoptosis rate of neurons, elevated expression of apoptosis-related proteins, and upregulated levels of inflammatory factors. However, miR-199a-5p overexpression/PRDM5 knockdown partially counteracted the effects of MALAT1 overexpression on H2O2-induced SCNs. In addition, MALAT1 negatively regulated miR-199a-5p, which targeted PRDM5.</p><p><strong>Conclusion: </strong>LncRNA MALAT1 promotes neuronal apoptosis during SCI by regulating the miR-199a-5p/PRDM5 axis.</p>","PeriodicalId":23395,"journal":{"name":"Turkish neurosurgery","volume":"1 1","pages":"196-205"},"PeriodicalIF":0.9000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LncRNA MALAT1 Promotes Neuronal Apoptosis During Spinal Cord Injury Through miR-199a-5p/ PRDM5 Axis.\",\"authors\":\"Xieli Guo, Huan Chen, Suonan Li, Shuai Zhang, Yong Gong, Jiangliu Yin\",\"doi\":\"10.5137/1019-5149.JTN.36175-21.5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aim: </strong>To determine the regulation of long non-coding RNA (lncRNA) MALAT1 on neuronal apoptosis during spinal cord injury (SCI) and to explore its possible mechanisms.</p><p><strong>Material and methods: </strong>The motor ability of SCI rat models and apoptosis in spinal cord tissue were evaluated. Primary spinal cord neurons (SCNs) were isolated and treated with H2O2 before cell transfection. The apoptosis of SCNs and expression of PRDM5 and MALAT1 were also measured. The interactions among MALAT1, miR-199a-5p, and PRDM5 were detected.</p><p><strong>Results: </strong>The motor ability of SCI rats decreased significantly. The proportion of apoptotic neurons increased in damaged tissue and SCN, along with an increase in the expression of apoptosis-related proteins c-caspase-3/9, autophagy-related proteins (p62 and LC3 II/I ratio), and proinflammatory factors. Moreover, overexpression of MALAT1 and PRDM5 in damaged SCN resulted in an increased apoptosis rate of neurons, elevated expression of apoptosis-related proteins, and upregulated levels of inflammatory factors. However, miR-199a-5p overexpression/PRDM5 knockdown partially counteracted the effects of MALAT1 overexpression on H2O2-induced SCNs. In addition, MALAT1 negatively regulated miR-199a-5p, which targeted PRDM5.</p><p><strong>Conclusion: </strong>LncRNA MALAT1 promotes neuronal apoptosis during SCI by regulating the miR-199a-5p/PRDM5 axis.</p>\",\"PeriodicalId\":23395,\"journal\":{\"name\":\"Turkish neurosurgery\",\"volume\":\"1 1\",\"pages\":\"196-205\"},\"PeriodicalIF\":0.9000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Turkish neurosurgery\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5137/1019-5149.JTN.36175-21.5\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish neurosurgery","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5137/1019-5149.JTN.36175-21.5","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
LncRNA MALAT1 Promotes Neuronal Apoptosis During Spinal Cord Injury Through miR-199a-5p/ PRDM5 Axis.
Aim: To determine the regulation of long non-coding RNA (lncRNA) MALAT1 on neuronal apoptosis during spinal cord injury (SCI) and to explore its possible mechanisms.
Material and methods: The motor ability of SCI rat models and apoptosis in spinal cord tissue were evaluated. Primary spinal cord neurons (SCNs) were isolated and treated with H2O2 before cell transfection. The apoptosis of SCNs and expression of PRDM5 and MALAT1 were also measured. The interactions among MALAT1, miR-199a-5p, and PRDM5 were detected.
Results: The motor ability of SCI rats decreased significantly. The proportion of apoptotic neurons increased in damaged tissue and SCN, along with an increase in the expression of apoptosis-related proteins c-caspase-3/9, autophagy-related proteins (p62 and LC3 II/I ratio), and proinflammatory factors. Moreover, overexpression of MALAT1 and PRDM5 in damaged SCN resulted in an increased apoptosis rate of neurons, elevated expression of apoptosis-related proteins, and upregulated levels of inflammatory factors. However, miR-199a-5p overexpression/PRDM5 knockdown partially counteracted the effects of MALAT1 overexpression on H2O2-induced SCNs. In addition, MALAT1 negatively regulated miR-199a-5p, which targeted PRDM5.
Conclusion: LncRNA MALAT1 promotes neuronal apoptosis during SCI by regulating the miR-199a-5p/PRDM5 axis.
期刊介绍：
Turkish Neurosurgery is a peer-reviewed, multidisciplinary, open access and totally free journal directed at an audience of neurosurgery physicians and scientists. The official language of the journal is English. The journal publishes original articles in the form of clinical and basic research. Turkish Neurosurgery will only publish studies that have institutional review board (IRB) approval and have strictly observed an acceptable follow-up period. With the exception of reference presentation, Turkish Neurosurgery requires that all manuscripts be prepared in accordance with the Uniform Requirements for Manuscripts Submitted to Biomedical Journals.
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