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<p>Research has shown that miR-142-3p is vital in numerous ischemic diseases and is strongly linked to apoptosis. The effects and precise mechanisms behind miR-142-3p in cerebral ischemia–reperfusion injury (CIRI) are not yet comprehensively elucidated. The results revealed significant repression in miR-142-3p and elevation in PICALM in the plasma of CIRI individuals. To explore further, middle cerebral artery occlusion (MCAO) rat models and oxygen–glucose deprivation/reoxygenation (OGDR)-induced SH-SY5Y cells were conducted. In brain tissue and SH-SY5Y cells, we employed qRT-PCR and Western blot (WB) to estimate miR-142-3p alongside PICALM expression. Notably, overexpression of miR-142-3p significantly minimized infarct areas and cell apoptosis in ischemic rats, as evidenced by TTC staining and immunohistochemistry. Similarly, miR-142-3p upregulation enhanced cell viability (CV) while suppressing SH-SY5Y cell death under OGDR conditions. The connection between miR-142-3p and PICALM was validated via TargetScan and a luciferase reporter assessment. Rescue experiments were performed to uncover PICALM's involvement in miR-142-3p regulation during ischemic injury. In the presence of OGDR, miR-142-3p overexpression significantly promoted PI3K/Akt pathway activation, but this was mitigated by PICALM overexpression. Overall, miR-142-3p might provide neuroprotective benefits during OGDR injury by affecting PICALM and stimulating PI3K/Akt signaling, rendering it a possible therapeutic CIRI target.</p>

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MiR- 142 - 3p Up-regulation Mitigates Cerebral Ischemia–reperfusion Injury by Targeting PICALM

  • 期刊论文

  • 发表日期：

    2025年4月24日

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  • Lili Xie,
  • Debin Yuan,
  • Qian Li,
  • Nan Gu,
  • Haicun Shi,
  • Jianguo Zhong,
  • Fuling Yan

摘要

Research has shown that miR-142-3p is vital in numerous ischemic diseases and is strongly linked to apoptosis. The effects and precise mechanisms behind miR-142-3p in cerebral ischemia–reperfusion injury (CIRI) are not yet comprehensively elucidated. The results revealed significant repression in miR-142-3p and elevation in PICALM in the plasma of CIRI individuals. To explore further, middle cerebral artery occlusion (MCAO) rat models and oxygen–glucose deprivation/reoxygenation (OGDR)-induced SH-SY5Y cells were conducted. In brain tissue and SH-SY5Y cells, we employed qRT-PCR and Western blot (WB) to estimate miR-142-3p alongside PICALM expression. Notably, overexpression of miR-142-3p significantly minimized infarct areas and cell apoptosis in ischemic rats, as evidenced by TTC staining and immunohistochemistry. Similarly, miR-142-3p upregulation enhanced cell viability (CV) while suppressing SH-SY5Y cell death under OGDR conditions. The connection between miR-142-3p and PICALM was validated via TargetScan and a luciferase reporter assessment. Rescue experiments were performed to uncover PICALM's involvement in miR-142-3p regulation during ischemic injury. In the presence of OGDR, miR-142-3p overexpression significantly promoted PI3K/Akt pathway activation, but this was mitigated by PICALM overexpression. Overall, miR-142-3p might provide neuroprotective benefits during OGDR injury by affecting PICALM and stimulating PI3K/Akt signaling, rendering it a possible therapeutic CIRI target.