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Deletion of YTHDF1 (not YTHDF3) reduced brain and gut damage after traumatic brain injury

Wei Zhao1, Ruzhi Li2, Xiang Zhong3

  • 1Department of Neurosurgery, The Fourth Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Neurological Research
|July 31, 2024
PubMed
Abstract

Insights

Deleting YTHDF1, but not YTHDF3, reduces brain and gut damage after traumatic brain injury (TBI). This finding highlights YTHDF1 as a potential therapeutic target for TBI.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Trauma Research

Background:

  • Traumatic brain injury (TBI) can cause significant brain and gut damage.
  • The roles of YTHDF1 and YTHDF3 in TBI-induced pathology are not fully understood.

Purpose of the Study:

  • To investigate the distinct roles of YTHDF1 and YTHDF3 in brain and gut damage following TBI.

Main Methods:

  • Generated YTHDF1 knockout (YTHDF1-/-) and YTHDF3 knockout (YTHDF3-/-) mice using CRISPR/Cas9.
  • Established a TBI model using controlled cortical impact (CCI).
  • Assessed brain and gut tissue damage, including edema, inflammation, and histopathological lesions, 3 days post-CCI.

Main Results:

  • YTHDF1-/- mice exhibited reduced cortical edema, brain inflammation, and gut histopathological lesions compared to wild-type (WT) mice.
  • YTHDF3-/- mice did not show significant differences in these damage markers compared to WT mice.

Conclusions:

  • YTHDF1 deficiency mitigates TBI-induced brain and gut damage.
  • YTHDF3 does not appear to play a similar protective role in this TBI model.
  • YTHDF1 represents a potential therapeutic target for reducing secondary injury after TBI.
Keywords:
YTHDF1YTHDF3brain-gut axism6Atraumatic brain injury

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