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NAD+ affects differentially expressed genes-MBOAT2-SLC25A21-SOX6 in experimental autoimmune encephalomyelitis model.

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Title: NAD+ affects differentially expressed genes-MBOAT2-SLC25A21-SOX6 in experimental autoimmune encephalomyelitis model.
Authors: Zeng, Xu (AUTHOR), Zhang, Kexue (AUTHOR), Liang, Ming (AUTHOR), Yu, Bin (AUTHOR), Zhang, Peng (AUTHOR), Mehmood, Arshad (AUTHOR), Zhang, Hongtian (AUTHOR)
Source: International Journal of Neuroscience. Jun2025, Vol. 135 Issue 6, p618-625. 8p.
Subjects: Demyelination, Gene expression, Nerve tissue, SOX transcription factors, Organs (Anatomy)
Abstract: Background: Nicotinamide adenine dinucleotide (NAD+) plays a key role in neuroinflammation and neurodegeneration and provides anti-inflammatory and neuroprotective effects in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Aim: In this study, we aimed to investigate whether NAD+ affects differentially expressed genes (DEGs) in splenocytes of EAE mice to reveal candidate genes for the pathogenesis of MS. Methods: The EAE model was used to perform an intervention on NAD+ to investigate its potential as a protective agent in inflammation and demyelination. Transcriptome analysis of nerve tissue was carried out to gain better insights into NAD+ function. Effects of NAD+ on DEGs in the splenocytes of EAE mice were investigated to determine its anti-inflammatory effect. Results: NAD+ in EAE mice showed the clinical score was significantly improved (EAE 3.190 ± 0.473 vs. NAD+ 2.049 ± 0.715). DEGs (MBOAT2, SLC25A21, and SOX6) between the EAE and the EAE + NAD+ groups showed that SOX6 was significantly improved after NAD+ treatment compared with the EAE group, and other indicators were improved but did not reach statistical significance. NAD+ exhibited clinical scores in EAE mice, and key inflammation was ameliorated in EAE mice spleen after NAD+ intervention, while transcriptome analysis between EAE and EAE + NAD+ groups showed several DEGs in the underlying mechanism. Conclusion: NAD+ on DEGs attenuates disease severity in EAE. Transcriptome analysis on nerve tissue reveals several protein targets in the underlying mechanisms. However, NAD+ does not significantly improve DEGs in the splenocytes of the EAE model. HIGHLIGHTS: MBOAT2, SLC25A21, and SOX6 show significant fold change in EAE mice, while SOX6 shows significantly lower expression in the EAE group and the EAE + NAD+ group compared with the Ctrl. NAD+ in the EAE model provides its protective role in inflammation and demyelination. NAD+ exhibits clinical scores in EAE mice. NAD+ does not significantly improve DEGs in splenocytes of the EAE. SIGNIFICANCE STATEMENT: MS is an inflammatory, autoimmune, and demyelinating disorder of the CNS. The spleen is the immune organ in the body and plays an important role in the pathogenesis of MS. The relationship between spleen mRNA expression and MS pathogenesis has not been investigated in EAE mice with NAD+. This study screens out a profile of the DEGs in the spleen of EAE mice. After RT-qPCR validation, SOX6 showed significantly lower expression in the EAE group and the EAE + NAD+ group compared with the healthy Ctrls. The findings provide a genetic perspective on the importance of spleen gene expressions on MS etiology. [ABSTRACT FROM AUTHOR]
Copyright of International Journal of Neuroscience is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Label: Title
  Group: Ti
  Data: NAD<superscript>+</superscript> affects differentially expressed genes-MBOAT2-SLC25A21-SOX6 in experimental autoimmune encephalomyelitis model.
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  Data: <searchLink fieldCode="AR" term="%22Zeng%2C+Xu%22">Zeng, Xu</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhang%2C+Kexue%22">Zhang, Kexue</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Liang%2C+Ming%22">Liang, Ming</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Yu%2C+Bin%22">Yu, Bin</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhang%2C+Peng%22">Zhang, Peng</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Mehmood%2C+Arshad%22">Mehmood, Arshad</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zhang%2C+Hongtian%22">Zhang, Hongtian</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22International+Journal+of+Neuroscience%22">International Journal of Neuroscience</searchLink>. Jun2025, Vol. 135 Issue 6, p618-625. 8p.
– Name: Subject
  Label: Subjects
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22Demyelination%22">Demyelination</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink><br /><searchLink fieldCode="DE" term="%22Nerve+tissue%22">Nerve tissue</searchLink><br /><searchLink fieldCode="DE" term="%22SOX+transcription+factors%22">SOX transcription factors</searchLink><br /><searchLink fieldCode="DE" term="%22Organs+%28Anatomy%29%22">Organs (Anatomy)</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background: Nicotinamide adenine dinucleotide (NAD+) plays a key role in neuroinflammation and neurodegeneration and provides anti-inflammatory and neuroprotective effects in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Aim: In this study, we aimed to investigate whether NAD+ affects differentially expressed genes (DEGs) in splenocytes of EAE mice to reveal candidate genes for the pathogenesis of MS. Methods: The EAE model was used to perform an intervention on NAD+ to investigate its potential as a protective agent in inflammation and demyelination. Transcriptome analysis of nerve tissue was carried out to gain better insights into NAD+ function. Effects of NAD+ on DEGs in the splenocytes of EAE mice were investigated to determine its anti-inflammatory effect. Results: NAD+ in EAE mice showed the clinical score was significantly improved (EAE 3.190 ± 0.473 vs. NAD+ 2.049 ± 0.715). DEGs (MBOAT2, SLC25A21, and SOX6) between the EAE and the EAE + NAD+ groups showed that SOX6 was significantly improved after NAD+ treatment compared with the EAE group, and other indicators were improved but did not reach statistical significance. NAD+ exhibited clinical scores in EAE mice, and key inflammation was ameliorated in EAE mice spleen after NAD+ intervention, while transcriptome analysis between EAE and EAE + NAD+ groups showed several DEGs in the underlying mechanism. Conclusion: NAD+ on DEGs attenuates disease severity in EAE. Transcriptome analysis on nerve tissue reveals several protein targets in the underlying mechanisms. However, NAD+ does not significantly improve DEGs in the splenocytes of the EAE model. HIGHLIGHTS: MBOAT2, SLC25A21, and SOX6 show significant fold change in EAE mice, while SOX6 shows significantly lower expression in the EAE group and the EAE + NAD+ group compared with the Ctrl. NAD+ in the EAE model provides its protective role in inflammation and demyelination. NAD+ exhibits clinical scores in EAE mice. NAD+ does not significantly improve DEGs in splenocytes of the EAE. SIGNIFICANCE STATEMENT: MS is an inflammatory, autoimmune, and demyelinating disorder of the CNS. The spleen is the immune organ in the body and plays an important role in the pathogenesis of MS. The relationship between spleen mRNA expression and MS pathogenesis has not been investigated in EAE mice with NAD+. This study screens out a profile of the DEGs in the spleen of EAE mice. After RT-qPCR validation, SOX6 showed significantly lower expression in the EAE group and the EAE + NAD+ group compared with the healthy Ctrls. The findings provide a genetic perspective on the importance of spleen gene expressions on MS etiology. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of International Journal of Neuroscience is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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      – Type: doi
        Value: 10.1080/00207454.2024.2313022
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      – Code: eng
        Text: English
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      Pagination:
        PageCount: 8
        StartPage: 618
    Subjects:
      – SubjectFull: Demyelination
        Type: general
      – SubjectFull: Gene expression
        Type: general
      – SubjectFull: Nerve tissue
        Type: general
      – SubjectFull: SOX transcription factors
        Type: general
      – SubjectFull: Organs (Anatomy)
        Type: general
    Titles:
      – TitleFull: NAD+ affects differentially expressed genes-MBOAT2-SLC25A21-SOX6 in experimental autoimmune encephalomyelitis model.
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            NameFull: Zeng, Xu
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            – D: 01
              M: 06
              Text: Jun2025
              Type: published
              Y: 2025
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