Spinal Cord Research Help
AboutCategoriesLatest ResearchContact
Subscribe
Spinal Cord Research Help

Making Spinal Cord Injury (SCI) Research Accessible to Everyone. Simplified summaries of the latest research, designed for patients, caregivers and anybody who's interested.

Quick Links

  • Home
  • About
  • Categories
  • Latest Research
  • Disclaimer

Contact

  • Contact Us
© 2025 Spinal Cord Research Help

All rights reserved.

  1. Home
  2. Research
  3. Immunology
  4. Reduced inflammation accompanies diminished myelin damage and repair in the NG2 null mouse spinal cord

Reduced inflammation accompanies diminished myelin damage and repair in the NG2 null mouse spinal cord

Journal of Neuroinflammation, 2011 · DOI: 10.1186/1742-2094-8-158 · Published: November 13, 2011

ImmunologyNeurologyGenetics

Simple Explanation

This study investigates the role of the NG2 proteoglycan in spinal cord demyelination and remyelination, processes relevant to multiple sclerosis (MS). NG2 is found on oligodendrocyte progenitor cells (OPCs), pericytes, and macrophages/microglia, all of which participate in myelin damage and repair. The researchers compared myelin damage and repair in wild type mice versus NG2 null mice (lacking NG2) after inducing demyelination in the spinal cord. They also examined how NG2 affects the behavior of OPCs, pericytes, and macrophages/microglia during these processes. The findings suggest that NG2 plays a complex role, influencing both the initial damage and the subsequent repair. Loss of NG2 leads to decreased proliferation of key cell types and a shift towards an anti-inflammatory environment, ultimately affecting the extent of myelin damage and repair.

Study Duration
6 weeks
Participants
Male wild type (NG2+/+) and NG2 null (NG2-/-) mice between the ages of 3-5 months
Evidence Level
Not specified

Key Findings

  • 1
    The initial volume of spinal cord demyelination in wild type mice is twice as large as in NG2 null mice, suggesting NG2 influences the initial damage phase.
  • 2
    Over the ensuing 5 weeks, myelin repair was significantly better in wild type mice compared to NG2 null mice, indicating NG2's importance in the repair process.
  • 3
    NG2 ablation resulted in reduced numbers and proliferation of OPCs, pericytes, and macrophages/microglia in demyelinated lesions, demonstrating NG2's role in regulating these cell populations.

Research Summary

This study examines the role of NG2, a proteoglycan expressed by OPCs, pericytes, and macrophages/microglia, in spinal cord demyelination and remyelination using wild type and NG2 null mice. Results showed that NG2 ablation leads to decreased proliferation of OPCs, pericytes, and macrophages/microglia, which reduces the abundance of all three cell types in demyelinated spinal cord lesions. The study concludes that NG2 is an important factor in regulating myelin processing, suggesting therapeutic targeting of the proteoglycan might offer a means of manipulating cell behavior in demyelinating diseases.

Practical Implications

Therapeutic Target

NG2 could be a potential therapeutic target for manipulating cell behavior in demyelinating diseases such as multiple sclerosis.

Cell-Specific Ablation

Cell type-specific ablation of NG2 will be a useful strategy for elucidating the respective contributions of NG2-positive cell types to the myelin damage and repair processes.

Understanding Myelin Repair

Further research into NG2's role in cell proliferation and motility could lead to a better understanding of myelin repair mechanisms.

Study Limitations

  • 1
    Global NG2 knockout may have pleiotropic effects.
  • 2
    Cell-specific contributions of NG2 are not fully elucidated.
  • 3
    The study focuses on lysolecithin-induced demyelination, which may not fully replicate the complexities of MS.

Your Feedback

Was this summary helpful?

Back to Immunology