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Related Experiment Video

Updated: Oct 25, 2025

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Hippocampal Transcriptome Changes After Subarachnoid Hemorrhage in Mice.

Angelique S Regnier-Golanov1, Friederike Dündar2, Paul Zumbo2

  • 1Laboratory of Cerebrovascular Research, Department of Neurosurgery, Houston Methodist Hospital, Houston, TX, United States.

Frontiers in Neurology
|August 6, 2021
PubMed
Summary

Subarachnoid hemorrhage (SAH) causes cognitive deficits by altering hippocampal gene expression. This study reveals suppressed oligodendrocyte function and activated immune responses, offering new therapeutic targets for post-SAH syndrome.

Keywords:
cognitive deficitscomplementhippocampusoligodendrocytepost-SAH syndromesubarachnoid hemorrhagetranscriptome

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genomics

Background:

  • Subarachnoid hemorrhage (SAH) frequently leads to long-term cognitive deficits, including memory impairment and emotional disturbances, collectively termed post-SAH syndrome.
  • The precise molecular mechanisms underlying these cognitive impairments, particularly the role of hippocampal changes, remain largely unknown despite their presumed link to temporomesial-hippocampal damage.

Purpose of the Study:

  • To systematically investigate the hippocampal gene expression profile following experimental subarachnoid hemorrhage (SAH) in a mouse model.
  • To identify specific molecular pathways and gene expression changes that contribute to the cognitive deficits observed in post-SAH syndrome.

Main Methods:

  • A mouse model of SAH was established by perforating the circle of Willis.
  • Whole bilateral hippocampi were collected four days post-SAH for RNA sequencing.
  • Differential gene expression analysis, functional enrichment (IPA, Gene Ontology, REACTOME, MsigDB), and motif analysis (MEME-Suite) were employed.

Main Results:

  • Significant differential expression of 642 upregulated and 398 downregulated genes was observed in the hippocampus of SAH mice compared to controls.
  • Key affected pathways included suppression of oligodendrocyte/myelin-related genes and overexpression of genes involved in the complement system, immunity, and extracellular matrix reorganization.
  • Interferon regulatory factors, TGF-β1, and BMP were identified as critical orchestrating factors, with specific transcription factor binding motifs (KLFs, ZNF, IRFs) enriched in gene promoters.

Conclusions:

  • This study presents the first comprehensive database of hippocampal gene and pathway responses after SAH.
  • Findings suggest that SAH can remotely trigger hippocampal responses, including impaired oligodendrocyte function, potentially mediated by entorhinal cortex damage.
  • The identified molecular pathways offer novel therapeutic targets for mitigating cognitive deficits associated with post-SAH syndrome.