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MiRNA-26a promotes angiogenesis in a rat model of cerebral infarction via PI3K/AKT and MAPK/ERK pathway

Z Liang1, Y-J Chi, G-Q Lin

  • 1Department of Neurosurgery, Lianjiang Hospital Affiliated To Guangdong Medical University/Lianjiang People's Hospital, Lianjiang, China. liangzaizai008@163.com.

European Review for Medical and Pharmacological Sciences
|June 20, 2018
PubMed
Abstract

Insights

MicroRNA-26a promotes blood vessel formation in rats after ischemic stroke. It activates signaling pathways to enhance cell growth and repair, aiding recovery from brain injury.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Cerebral ischemic stroke remains a leading cause of disability.
  • Understanding the molecular mechanisms of angiogenesis is crucial for developing effective treatments.
  • MicroRNAs play significant roles in regulating cellular processes relevant to stroke recovery.

Purpose of the Study:

  • To investigate the specific role of microRNA-26a (miRNA-26a) in a rat model of cerebral ischemic stroke.
  • To elucidate the underlying molecular mechanisms by which miRNA-26a influences angiogenesis and cell proliferation.

Main Methods:

  • Established a rat model of middle cerebral artery occlusion (MCAO) to induce cerebral infarction.
  • Quantified miRNA-26a expression using qPCR in brain tissue and brain microvascular endothelial cells (BMECs).
  • Assessed endothelial lumen formation, cell proliferation (MTT assay), and signaling pathway activation (Western blot for PI3K/AKT and MAPK/ERK).

Main Results:

  • miRNA-26a expression was significantly elevated following cerebral infarction.
  • miRNA-26a mimics promoted endothelial lumen formation and BMEC proliferation, while inhibitors reduced these effects.
  • miRNA-26a was found to up-regulate HIF-1a via the AKT and ERK1/2 pathways, subsequently promoting VEGF transcription.

Conclusions:

  • miRNA-26a plays a critical role in promoting angiogenesis post-cerebral ischemic stroke.
  • The pro-angiogenic effects of miRNA-26a are mediated through the PI3K/AKT and MAPK/ERK signaling pathways.
  • Targeting miRNA-26a may represent a therapeutic strategy for enhancing recovery after ischemic stroke.

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