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<p>Signal Transducer and Activator of Transcription 1 (STAT1) is a nuclear transcription factor involved in multiple biological processes including the cell cycle, cell survival and immune response. However, the role and mechanism of STAT1 overexpression in learning and memory of young mice have not been investigated. Here, we indicated that STAT1 overexpression apparently induced cognitive defects of 2-month-old C57 mice. STAT1 overexpression in 2-month-old C57 mice markedly decreased spine density and the levels of synaptic associated protein including PSD95, SYN I and PSD93. Moreover, neuronal apoptosis was remarkably induced in STAT1-overexpression 2-month-old C57 mice by BCL-2/Bax signaling pathway. Furthermore, STAT1 overexpression in 2-month-old C57 mice apparently increased the proliferation of microglia and astrocytes, accompanied by a notable elevation in the mRNA levels of inflammatory factors including TNF-α, IL-1α, IL-6 and IL-18. In addition, STAT1 overexpression in 2-month-old C57 mice impaired mitochondrial function by increasing lipid peroxidation levels, decreasing ATP levels and superoxide dismutase activity. Proteomic analysis showed that protein expression profile of synapses, inflammation and mitochondria were all altered and that biological process of synaptic transmission, inflammatory response and fatty acid beta-oxidation were regulated via overexpressing STAT1 in 2-month-old C57 mice. Taken together, these findings suggest that STAT1 may be a pivotal risk factor for impaired cognitive ability.</p>

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Proteomics revealed the underlying mechanism of STAT1-induced cognitive deficits in 2-month-old C57 mice

  • 期刊论文

  • 发表日期：

    2025年11月14日

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  • Xiao Li,
  • Ting Li,
  • Bocheng Xiong,
  • Juan Luo,
  • Xifei Yang,
  • Yan Feng

摘要

Signal Transducer and Activator of Transcription 1 (STAT1) is a nuclear transcription factor involved in multiple biological processes including the cell cycle, cell survival and immune response. However, the role and mechanism of STAT1 overexpression in learning and memory of young mice have not been investigated. Here, we indicated that STAT1 overexpression apparently induced cognitive defects of 2-month-old C57 mice. STAT1 overexpression in 2-month-old C57 mice markedly decreased spine density and the levels of synaptic associated protein including PSD95, SYN I and PSD93. Moreover, neuronal apoptosis was remarkably induced in STAT1-overexpression 2-month-old C57 mice by BCL-2/Bax signaling pathway. Furthermore, STAT1 overexpression in 2-month-old C57 mice apparently increased the proliferation of microglia and astrocytes, accompanied by a notable elevation in the mRNA levels of inflammatory factors including TNF-α, IL-1α, IL-6 and IL-18. In addition, STAT1 overexpression in 2-month-old C57 mice impaired mitochondrial function by increasing lipid peroxidation levels, decreasing ATP levels and superoxide dismutase activity. Proteomic analysis showed that protein expression profile of synapses, inflammation and mitochondria were all altered and that biological process of synaptic transmission, inflammatory response and fatty acid beta-oxidation were regulated via overexpressing STAT1 in 2-month-old C57 mice. Taken together, these findings suggest that STAT1 may be a pivotal risk factor for impaired cognitive ability.