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A Murine Model of Subarachnoid Hemorrhage
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A Murine Model of Subarachnoid Hemorrhage

Published on: November 21, 2013

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Neuroprotective effects of p53/microRNA‑22 regulate inflammation and apoptosis in subarachnoid hemorrhage

Shui Yu1, Yi-Jun Zeng1, Xiao-Chuan Sun1

  • 1Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.

International Journal of Molecular Medicine
|January 17, 2018
PubMed

Insights

The p53/microRNA-22 pathway plays a crucial role in regulating inflammation and apoptosis following subarachnoid hemorrhage (SAH). This study reveals its neuroprotective potential in managing SAH-induced brain injury.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Subarachnoid hemorrhage (SAH) is a critical neurological condition characterized by inflammation and neuronal apoptosis.
  • The roles of p53 and microRNA-22 in SAH pathogenesis require further elucidation.

Purpose of the Study:

  • To investigate the neuroprotective mechanisms of p53/microRNA-22 in regulating inflammation and apoptosis in a mouse model of SAH.
  • To explore the interplay between p53 and microRNA-22 in the context of SAH.

Main Methods:

  • Subarachnoid hemorrhage was induced in a mouse model.
  • MicroRNA-22 and p53 expression levels were analyzed using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot.
  • In vitro experiments using HEB cells were conducted to assess the effects of p53 inhibition and knockdown on inflammatory and apoptotic markers.
  • Key proteins such as Bax and Cyr61 were quantified via western blot analysis.

Main Results:

  • MicroRNA-22 expression was upregulated in the SAH mouse model.
  • Downregulation of microRNA-22 in HEB cells increased interleukin-6 (IL-6) and cysteine-rich angiogenic inducer 61 (Cyr61) expression while decreasing B-cell lymphoma 2-associated X protein (Bax) and caspase-3 activity.
  • Inhibition or knockdown of p53 led to increased IL-6, decreased microRNA-22, suppressed Bax protein, and reduced caspase-3 activity, with induced Cyr61 expression in both in vivo and in vitro models.

Conclusions:

  • The p53/microRNA-22 axis demonstrates significant neuroprotective effects in SAH by modulating inflammation and apoptosis.
  • Targeting the p53/microRNA-22 pathway may offer a therapeutic strategy for managing brain injury after subarachnoid hemorrhage.

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