Scholarlink

<p>The objective of this study was to elucidate the molecular mechanisms by which cAMP-regulated transcription coactivator1 (CRTC1) regulates autophagy and GluA2 expression in patients with epilepsy. Methods: We initially established a magnesium-free epilepsy cell model and recorded cellular discharges using the whole-cell patch clamp technique. Next, we experimentally activated autophagy and identified effective methods for silencing the CRTC1 gene using RNA interference technology. Furthermore, we developed an animal models of status epilepticus and employed immunofluorescence and Western Blot to elucidate CRTC1’s role in regulating autophagy-related genes and GluA2 expression in epilepsy. Results: We observed mouse hippocampal neurons under magnesium-free extracellular conditions. Treatment with an autophagy activator decreased GluA2 expression; however, CRTC1 was not dephosphorylated. CRTC1 siRNA suppressed LC3 and PSD95 expression, whereas CRTC1&#xa0;siRNA intervention restored GluA2 expression. Conclusion: CRTC1 indirectly influences the expression of synaptic-related proteins and GluA2 by directly modulating autophagy during the pathological process of epilepsy. The findings of this study reveal novel molecular targets for the treatment of epilepsy.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Regulatory Mechanism of CRTC1 on Autophagy and GluA2 Expression in Epilepsy

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月10日

查看全文
  • Xueying Wang,
  • Liqian Zhou,
  • Lin Yang,
  • Shaoping Huang,
  • Yuying Wang,
  • Dan Li

摘要

The objective of this study was to elucidate the molecular mechanisms by which cAMP-regulated transcription coactivator1 (CRTC1) regulates autophagy and GluA2 expression in patients with epilepsy. Methods: We initially established a magnesium-free epilepsy cell model and recorded cellular discharges using the whole-cell patch clamp technique. Next, we experimentally activated autophagy and identified effective methods for silencing the CRTC1 gene using RNA interference technology. Furthermore, we developed an animal models of status epilepticus and employed immunofluorescence and Western Blot to elucidate CRTC1’s role in regulating autophagy-related genes and GluA2 expression in epilepsy. Results: We observed mouse hippocampal neurons under magnesium-free extracellular conditions. Treatment with an autophagy activator decreased GluA2 expression; however, CRTC1 was not dephosphorylated. CRTC1 siRNA suppressed LC3 and PSD95 expression, whereas CRTC1 siRNA intervention restored GluA2 expression. Conclusion: CRTC1 indirectly influences the expression of synaptic-related proteins and GluA2 by directly modulating autophagy during the pathological process of epilepsy. The findings of this study reveal novel molecular targets for the treatment of epilepsy.