Tuan Anh Pham, Takashi Sakai, Huy Van Dang, Diem Hong Tran, Yuji Shishido, Nam Hoang Tran, Kiyoshi Fukui
{"title":"成核是一种与凋亡相关的应激诱导蛋白,对脑神经炎症中的小胶质细胞极化/激活很重要。","authors":"Tuan Anh Pham, Takashi Sakai, Huy Van Dang, Diem Hong Tran, Yuji Shishido, Nam Hoang Tran, Kiyoshi Fukui","doi":"10.1093/jb/mvaf055","DOIUrl":null,"url":null,"abstract":"<p><p>Microglia, the central nervous system's resident macrophages, are critical for immune defense, protecting neurons during infection. Their role in postnatal brain development, particularly after injury, remains unclear. Nucling, a protein up-regulated during cardiac muscle differentiation, regulates NF-κB, influencing apoptosis and cell proliferation. In this study, we examined the role of Nucling in microglial activation using wild-type (WT) and Nucling-knockout (KO) neonatal mice subjected to poly(I:C), a viral mimic. Poly(I:C) treatment increased Iba1-positive microglia in both genotypes; however, KO mice showed a significantly exaggerated response in both cortical and hippocampal regions. Furthermore, while pro-inflammatory M1 markers (iNOS, CD86, TNFα, IL-6) were upregulated in both WT and KO mice, the anti-inflammatory M2 marker Arginase 1 (Arg1) was induced in WT but significantly suppressed in KO mice, indicating impaired M2 polarization. These findings suggest Nucling is essential for maintaining microglial polarization, supporting immunological processes against pathogens, and aiding central nervous system development.</p>","PeriodicalId":15234,"journal":{"name":"Journal of biochemistry","volume":" ","pages":""},"PeriodicalIF":1.7000,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Nucling, a stress-inducible protein associated with apoptosomes, is important for microglial polarization/activation in the brain neuroinflamation.\",\"authors\":\"Tuan Anh Pham, Takashi Sakai, Huy Van Dang, Diem Hong Tran, Yuji Shishido, Nam Hoang Tran, Kiyoshi Fukui\",\"doi\":\"10.1093/jb/mvaf055\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Microglia, the central nervous system's resident macrophages, are critical for immune defense, protecting neurons during infection. Their role in postnatal brain development, particularly after injury, remains unclear. Nucling, a protein up-regulated during cardiac muscle differentiation, regulates NF-κB, influencing apoptosis and cell proliferation. In this study, we examined the role of Nucling in microglial activation using wild-type (WT) and Nucling-knockout (KO) neonatal mice subjected to poly(I:C), a viral mimic. Poly(I:C) treatment increased Iba1-positive microglia in both genotypes; however, KO mice showed a significantly exaggerated response in both cortical and hippocampal regions. Furthermore, while pro-inflammatory M1 markers (iNOS, CD86, TNFα, IL-6) were upregulated in both WT and KO mice, the anti-inflammatory M2 marker Arginase 1 (Arg1) was induced in WT but significantly suppressed in KO mice, indicating impaired M2 polarization. These findings suggest Nucling is essential for maintaining microglial polarization, supporting immunological processes against pathogens, and aiding central nervous system development.</p>\",\"PeriodicalId\":15234,\"journal\":{\"name\":\"Journal of biochemistry\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2025-09-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of biochemistry\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1093/jb/mvaf055\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biochemistry","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1093/jb/mvaf055","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Nucling, a stress-inducible protein associated with apoptosomes, is important for microglial polarization/activation in the brain neuroinflamation.
Microglia, the central nervous system's resident macrophages, are critical for immune defense, protecting neurons during infection. Their role in postnatal brain development, particularly after injury, remains unclear. Nucling, a protein up-regulated during cardiac muscle differentiation, regulates NF-κB, influencing apoptosis and cell proliferation. In this study, we examined the role of Nucling in microglial activation using wild-type (WT) and Nucling-knockout (KO) neonatal mice subjected to poly(I:C), a viral mimic. Poly(I:C) treatment increased Iba1-positive microglia in both genotypes; however, KO mice showed a significantly exaggerated response in both cortical and hippocampal regions. Furthermore, while pro-inflammatory M1 markers (iNOS, CD86, TNFα, IL-6) were upregulated in both WT and KO mice, the anti-inflammatory M2 marker Arginase 1 (Arg1) was induced in WT but significantly suppressed in KO mice, indicating impaired M2 polarization. These findings suggest Nucling is essential for maintaining microglial polarization, supporting immunological processes against pathogens, and aiding central nervous system development.
期刊介绍:
The Journal of Biochemistry founded in 1922 publishes the results of original research in the fields of Biochemistry, Molecular Biology, Cell, and Biotechnology written in English in the form of Regular Papers or Rapid Communications. A Rapid Communication is not a preliminary note, but it is, though brief, a complete and final publication. The materials described in Rapid Communications should not be included in a later paper. The Journal also publishes short reviews (JB Review) and papers solicited by the Editorial Board.