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Related Experiment Video

Updated: Aug 20, 2025

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Neuroinflammation after ischemic stroke involves INPP5D expression mediated by the TMPO-AS1-PU.1 complex.

Wenhui Luan1, Zhongwen Sun2, Chunmei Wu1

  • 1Neurology Department EEG Room, Yantai Yuhuangding Hospital, Yantai 264000, China.

Neurological Research
|November 23, 2022
PubMed
Summary

Long non-coding RNA TMPO-AS1 exacerbates ischemic stroke by promoting neuroinflammation. Inhibiting TMPO-AS1 reduces inflammation and infarct volume, improving neurological function in a mouse model.

Keywords:
BV2 cellsINPP5DIschemic strokePU.1TMPO-AS1

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Ischemic stroke is a leading cause of death and disability worldwide.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in various diseases, including stroke.
  • The specific role of lncRNA TMPO-AS1 in ischemic stroke pathogenesis remains largely unexplored.

Purpose of the Study:

  • To investigate the role of lncRNA TMPO-AS1 in ischemic stroke.
  • To elucidate the underlying molecular mechanisms by which TMPO-AS1 influences neuroinflammation and stroke outcomes.

Main Methods:

  • Established a middle cerebral artery occlusion (MCAO) mouse model of ischemic stroke.
  • Utilized hypoxia/glucose deprivation/reoxygenation (OGD/R) in BV2 cells to mimic ischemic conditions.
  • Interfered with TMPO-AS1 expression using shRNA lentivirus and assessed protein and gene expression, inflammatory cytokine secretion, and cell viability.
  • Employed RNA immunoprecipitation (RIP), PNA-pull down, luciferase reporter, and chromatin immunoprecipitation (ChIP) assays to determine molecular interactions and transcriptional activity.

Main Results:

  • TMPO-AS1 levels were elevated in ischemic stroke patients, MCAO mice, and OGD/R-induced BV2 cells.
  • TMPO-AS1 interference significantly inhibited neuroinflammation in OGD/R-induced BV2 cells.
  • TMPO-AS1 enhanced nuclear accumulation of PU.1 by binding to it, thereby promoting INPP5D transcription.
  • Overexpression of INPP5D reversed the anti-inflammatory effects of TMPO-AS1 interference.
  • TMPO-AS1 interference reduced infarct volume and improved sensorimotor and cognitive functions in MCAO mice.

Conclusions:

  • lncRNA TMPO-AS1 plays a critical role in exacerbating neuroinflammation and stroke progression.
  • The TMPO-AS1-PU.1 complex promotes INPP5D expression, contributing to stroke pathology.
  • Targeting TMPO-AS1 represents a potential therapeutic strategy for ischemic stroke.