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YTHDF1 Attenuates TBI-Induced Brain-Gut Axis Dysfunction in Mice.

Peizan Huang1,2,3, Min Liu2, Jing Zhang2

  • 1Department of Neurosurgery, Shanghai East Hospital, Nanjing Medical University, Shanghai 200120, China.

International Journal of Molecular Sciences
|February 25, 2023
PubMed
Summary

YTHDF1 knockout reduces brain and gut damage after traumatic brain injury (TBI). This intervention improves gut microbiome balance and may offer a new therapeutic strategy for TBI-related brain-gut axis dysfunction.

Keywords:
YTHDF1brain-gut axism6A RNA modificationmicrobiotatraumatic brain injury

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Area of Science:

  • Neuroscience
  • Gastroenterology
  • Molecular Biology

Background:

  • The brain-gut axis (BGA) facilitates bidirectional communication between the brain and gut.
  • Traumatic brain injury (TBI) can disrupt BGA function through neuroinflammation and neurotoxicity.
  • N6-methyladenosine (m6A) RNA modification plays roles in both brain and gut, but its involvement in TBI-induced BGA dysfunction is unknown.

Purpose of the Study:

  • To investigate the role of m6A RNA methylation, specifically the YTHDF1 protein, in TBI-induced BGA dysfunction.
  • To determine if YTHDF1 knockout affects TBI-related pathological changes, inflammation, apoptosis, and gut microbiome composition.

Main Methods:

  • Traumatic brain injury was induced in mice using the controlled cortical impact (CCI) model.
  • YTHDF1 knockout mice and wild-type (WT) littermates were used.
  • Histopathological, biochemical, and microbiome analyses were performed on brain and gut tissues.
  • Differential gene expression analysis was conducted on cortical tissues.

Main Results:

  • YTHDF1 knockout significantly reduced brain and gut histopathological lesions, apoptosis, inflammation, and edema proteins post-TBI.
  • YTHDF1 knockout improved fungal mycobiome abundance and enhanced colonization of beneficial probiotics, notably Akkermansia, at 3 days post-CCI.
  • Gene expression analysis revealed enrichment of neurotransmitter, inflammatory, and apoptotic signaling pathways in YTHDF1-deficient brains.
  • The ITGA6-mediated cell adhesion molecule signaling pathway was identified as a key m6A regulatory pathway in TBI-induced BGA dysfunction.

Conclusions:

  • YTHDF1 plays a critical role in TBI-induced brain-gut axis dysfunction.
  • YTHDF1 knockout demonstrates a protective effect against TBI-induced damage and BGA disruption.
  • Targeting YTHDF1 or m6A modification pathways may represent a novel therapeutic approach for managing TBI and its associated gut complications.