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<p>This study aimed to investigate the expression and role of Signaling Lymphocytic Activation Molecule Family Member 8 (SLAMF8) in Alzheimer’s disease (AD), particularly its interaction with NINJ2 in the TLR4/NF-κB signaling pathway. SLAMF8 expression levels in AD models were analyzed using the Gene Expression Omnibus (GEO) database. Validation of SLAMF8 expression was conducted through RT-PCR and Western blot in Aβ<sub>1−42</sub>-exposed SH-SY5Y cells, LPS-exposed HMC3 cells, and APP/PS1 transgenic mice. The interaction between SLAMF8 and NINJ2 was explored through co-immunoprecipitation, confocal immunofluorescence, and Western blot analyses, focusing on their roles in the TLR4/NF-κB signaling pathway. SLAMF8 was significantly upregulated in AD models, and its overexpression activated the TLR4/NF-κB signaling pathway, leading to increased levels of pro-inflammatory cytokines and oxidative stress. NINJ2 was identified as a direct functional partner of SLAMF8, with co-localization observed in the cytoplasm. Knockout of NINJ2 abolished SLAMF8-mediated activation of the TLR4/NF-κB pathway, neuroinflammation, and oxidative stress. The SLAMF8-NINJ2-TLR4/NF-κB axis is a crucial signaling pathway in AD progression. SLAMF8 and NINJ2 emerge as potential therapeutic targets for managing AD, with significant implications for future research and clinical interventions.</p>

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SLAMF8 and NINJ2 promote neuroinflammation and oxidative stress through TLR4 NF kappa B pathway in Alzheimer’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月20日

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  • Shuo Liu,
  • Yuze He,
  • He Chen,
  • Wenwen Zhao,
  • Heman Xu,
  • Tao Bai,
  • Juan Feng

摘要

This study aimed to investigate the expression and role of Signaling Lymphocytic Activation Molecule Family Member 8 (SLAMF8) in Alzheimer’s disease (AD), particularly its interaction with NINJ2 in the TLR4/NF-κB signaling pathway. SLAMF8 expression levels in AD models were analyzed using the Gene Expression Omnibus (GEO) database. Validation of SLAMF8 expression was conducted through RT-PCR and Western blot in Aβ1−42-exposed SH-SY5Y cells, LPS-exposed HMC3 cells, and APP/PS1 transgenic mice. The interaction between SLAMF8 and NINJ2 was explored through co-immunoprecipitation, confocal immunofluorescence, and Western blot analyses, focusing on their roles in the TLR4/NF-κB signaling pathway. SLAMF8 was significantly upregulated in AD models, and its overexpression activated the TLR4/NF-κB signaling pathway, leading to increased levels of pro-inflammatory cytokines and oxidative stress. NINJ2 was identified as a direct functional partner of SLAMF8, with co-localization observed in the cytoplasm. Knockout of NINJ2 abolished SLAMF8-mediated activation of the TLR4/NF-κB pathway, neuroinflammation, and oxidative stress. The SLAMF8-NINJ2-TLR4/NF-κB axis is a crucial signaling pathway in AD progression. SLAMF8 and NINJ2 emerge as potential therapeutic targets for managing AD, with significant implications for future research and clinical interventions.