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<p>Cerebral ischemia-reperfusion injury (CI/RI) remains a significant challenge in ischemic stroke treatment, often leading to exacerbated neuronal apoptosis and poor neurological recovery despite successful recanalization. MicroRNAs (miRNAs) are known to influence neurodegeneration and repair through post-transcriptional modulation of apoptosis-related genes. In this study, we investigated the neuroprotective role of miR-132 and its interaction with the epigenetic regulator Mecp2 under CI/RI conditions. Utilizing a rat MCAO model and SH-SY5Y neuronal cells exposed to OGD/R, we found that miR-132 levels were significantly decreased while Mecp2 expression was elevated following ischemic injury. Functional assays revealed that overexpression of miR-132 restored neuronal viability, increased anti-apoptotic Bcl-2, and reduced pro-apoptotic Bax expression. In contrast, inhibition of miR-132 exacerbated apoptosis. Bioinformatic analysis and dual-luciferase reporter assays confirmed that miR-132 directly targets the 3′UTR of Mecp2. Importantly, Mecp2 overexpression abolished the protective effects of miR-132, indicating that this axis is essential for apoptosis modulation. These findings establish the miR-132/Mecp2 axis as a key determinant of neuronal fate in CI/RI and identify it as a promising target for neuroprotective therapies.</p>

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MicroRNA-132 Alleviates Ischemia-Reperfusion-Induced Neuronal Apoptosis by Targeting Mecp2 in Stroke Models

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月16日

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  • Xiang Wang,
  • Rui Ma,
  • Zilu Liu,
  • Wenjin Sun,
  • Lin Xia,
  • Yurou Wang,
  • Donghua Shao,
  • Caixia Sun

摘要

Cerebral ischemia-reperfusion injury (CI/RI) remains a significant challenge in ischemic stroke treatment, often leading to exacerbated neuronal apoptosis and poor neurological recovery despite successful recanalization. MicroRNAs (miRNAs) are known to influence neurodegeneration and repair through post-transcriptional modulation of apoptosis-related genes. In this study, we investigated the neuroprotective role of miR-132 and its interaction with the epigenetic regulator Mecp2 under CI/RI conditions. Utilizing a rat MCAO model and SH-SY5Y neuronal cells exposed to OGD/R, we found that miR-132 levels were significantly decreased while Mecp2 expression was elevated following ischemic injury. Functional assays revealed that overexpression of miR-132 restored neuronal viability, increased anti-apoptotic Bcl-2, and reduced pro-apoptotic Bax expression. In contrast, inhibition of miR-132 exacerbated apoptosis. Bioinformatic analysis and dual-luciferase reporter assays confirmed that miR-132 directly targets the 3′UTR of Mecp2. Importantly, Mecp2 overexpression abolished the protective effects of miR-132, indicating that this axis is essential for apoptosis modulation. These findings establish the miR-132/Mecp2 axis as a key determinant of neuronal fate in CI/RI and identify it as a promising target for neuroprotective therapies.