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TSG-6-Mediated Extracellular Matrix Modifications Regulate Hypoxic-Ischemic Brain Injury.

Taasin Srivastava1, Hung Nguyen2, Gage Haden3

  • 1Department of Pediatrics, Oregon Health and Science University (OHSU), Portland, Oregon 97239 srivasta@ohsu.edu backs@ohsu.edu.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|April 3, 2024
PubMed
Summary

TNFα-stimulated gene-6 (TSG-6) modifies brain extracellular matrix (ECM) hyaluronic acid (HA) to regulate the Hippo-YAP1 pathway. This TSG-6-dependent ECM modification controls age- and sex-dependent responses to hypoxic-ischemic (H-I) brain injury.

Keywords:
extracellular matrixhypoxic–ischemic injurylink-domain proteoglycanneonatal brain injurysignal transduction

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Area of Science:

  • Neuroscience
  • Extracellular Matrix Biology
  • Developmental Biology

Background:

  • Proteoglycans regulate extracellular matrix (ECM) homeostasis and tissue response to injury.
  • Hypoxic-ischemic (H-I) injury disrupts brain homeostasis.
  • The role of hyaluronic acid (HA) modifications in the brain's response to H-I injury is unknown.

Purpose of the Study:

  • To investigate the role of TNFα-stimulated gene-6 (TSG-6) in modifying brain ECM hyaluronic acid (HA).
  • To determine if TSG-6-mediated ECM modifications regulate the Hippo-YAP1 pathway during neurodevelopment and in response to H-I injury.
  • To examine the age- and sex-dependent effects of TSG-6 deficiency on H-I injury outcomes.

Main Methods:

  • Utilized male and female mice lacking TSG-6 expression (TSG-6-/-).
  • Analyzed ECM HA modifications by TSG-6 during neurodevelopmental windows.
  • Assessed Hippo-YAP1 pathway activity and expression of YAP1 targets (EAAT1, EAAT2).
  • Evaluated brain response to H-I injury in TSG-6-/- mice at different ages and sexes.

Main Results:

  • TSG-6 is active in the brain from birth, differentially modifying ECM HA during development.
  • TSG-6-dependent ECM HA modifications regulate Hippo-YAP1 pathway activity.
  • TSG-6-/- mice exhibit dysregulated YAP1 target expression (EAAT1, EAAT2).
  • TSG-6 deficiency leads to age- and sex-dependent sensitization to H-I injury, with neonates showing anti-inflammatory and adult males showing pro-inflammatory responses.

Conclusions:

  • TSG-6-dependent ECM HA modifications act as a developmental switch regulating the Hippo-YAP1 pathway in the brain.
  • The Hippo-YAP1 pathway, modulated by TSG-6 and ECM, is a key regulator of age- and sex-dependent brain injury responses.
  • Findings highlight TSG-6 as a critical factor in brain homeostasis and injury resilience.