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Updated: Jan 7, 2026

A Neurosphere Assay to Evaluate Endogenous Neural Stem Cell Activation in a Mouse Model of Minimal Spinal Cord Injury
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A Neurosphere Assay to Evaluate Endogenous Neural Stem Cell Activation in a Mouse Model of Minimal Spinal Cord Injury

Published on: September 13, 2018

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Rictor/mTORC2 signaling pathway protects endogenous neural stem cells to promote recovery after spinal cord injury

Kuileung Tong1,2, Shiming Li3, Guoliang Chen4

  • 1Guangdong Provincial Biomedical Innovation Platform of Regeneration and Repair of Spinal Cord and Nerve Injury, Department of Orthopedic Surgery, Shenzhen Key Laboratory of Bone Tissue Repair and Translational Research, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong Province, China.

Neural Regeneration Research
|December 30, 2025
PubMed
Abstract

No abstract available in PubMed .

Insights

Rapamycin-insensitive companion of mTOR (Rictor) protects neural stem cells from death after spinal cord injury. Enhancing Rictor activity may improve spinal cord injury repair and functional recovery.

Area of Science:

  • Neuroscience
  • Regenerative Medicine
  • Cell Biology

Background:

  • Endogenous neural stem cells are crucial for spinal cord injury (SCI) repair.
  • Inflammatory environments in SCI lesions often cause neural stem cell death via necroptosis.
  • The role of Rictor (Rapamycin-insensitive companion of mTOR), a component of mTORC2, in neural stem cell survival post-SCI is unknown.

Purpose of the Study:

  • To investigate the role of Rictor in endogenous neural stem cell survival and function following spinal cord injury.
  • To determine if Rictor signaling protects neural stem cells from necroptosis in the context of SCI.

Main Methods:

  • Generated conditional neural stem cell-specific Rictor knockout mice using the Cre-loxP system.
  • Assessed spinal cord morphology, function, and inflammatory responses post-SCI.
  • Utilized lentiviral-mediated Rictor knockdown in neural stem cells in vitro to examine lysosomal function and necroptosis sensitivity.

Main Results:

  • Neural stem cell-specific Rictor knockout mice showed impaired functional recovery after SCI compared to wild-type controls.
  • Rictor knockout correlated with increased inflammation and neural stem cell necroptosis susceptibility.
  • In vitro Rictor knockdown impaired lysosomal function and increased sensitivity to necroptosis-inducing agents.

Conclusions:

  • Rictor/mTORC2 signaling is essential for protecting endogenous neural stem cells against necroptosis after spinal cord injury.
  • Modulating Rictor activity presents a potential therapeutic strategy for enhancing neural stem cell survival and promoting functional recovery in SCI.
Keywords:
RIPK1Rictorendogenous neural stem cellglial scarinflammationlysosomemTORC2necroptosisspinal cord injury

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