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MiR-155 deletion reduces ischemia-induced paralysis in an aortic aneurysm repair mouse model: Utility of immunohistochemistry and histopathology in understanding etiology of spinal cord paralysis

Ann Diagn Pathol, 2018 · DOI: 10.1016/j.anndiagpath.2018.06.002 · Published: October 1, 2018

Spinal Cord InjuryCardiovascular ScienceGenetics

Simple Explanation

Spinal cord paralysis is a common complication after surgery to repair thoraco-abdominal aortic aneurysms (TAAA). This study examines the causes of this paralysis, focusing on the role of a molecule called miR-155. The researchers found that in mice, deleting miR-155 reduced spinal cord damage and paralysis caused by interrupted blood flow during surgery. They observed that miR-155 affects the integrity of the blood-brain barrier, potentially worsening the damage. The study suggests that miR-155 could be a target for new treatments to prevent spinal cord injury during TAAA repair. It also highlights that diagnostic pathologists can use immunohistochemistry to determine if this mechanism is important in other ischemic diseases of the central nervous system, including stroke.

Study Duration
Not specified
Participants
Mice (wild-type and miR-155 knockout) and two human patients
Evidence Level
Level 3; Animal Study and Case Series

Key Findings

  • 1
    Increased miR-155 expression in neurons and endothelial cells of the spinal cord is associated with paralysis in a mouse model of aortic cross-clamping (ACC).
  • 2
    Deletion of miR-155 reduces central cord edema and the incidence of paralysis in ACC mice, suggesting that miR-155 activity accelerates the development of edema and spreading of gray matter damage.
  • 3
    MiR-155 targets Mfsd2a transcripts in neurons and endothelial cells, and miR-155 deletion increases Mfsd2a protective effects in ischemic cords.

Research Summary

This study investigates the role of miR-155 in spinal cord paralysis following aortic cross-clamping (ACC) in mice. The findings indicate that miR-155 contributes to gray matter edema and paralysis by targeting Mfsd2a in neurons and endothelial cells. Deletion of miR-155 reduced the incidence of paralysis and slowed the progression of central cord edema (CCE). The study suggests that miR-155 is instrumental in increasing the risk and accelerating the development of ACC-induced paralysis, and targeting miR-155 may have therapeutic potential.

Practical Implications

Therapeutic Target

MiR-155 may be a therapeutic target for preventing and treating spinal cord injury following TAAA repair.

Diagnostic Biomarker

Increased miR-155 and/or reduced Mfsd2a in neurons and endothelial cells can serve as biomarkers of ischemia-induced spinal cord damage.

Clinical Relevance

The mouse model used in this study closely mimics the patterns of gray matter edema observed in human patients after TAAA surgery, making it relevant for studying molecular mechanisms of spinal cord damage.

Study Limitations

  • 1
    The study is primarily based on a mouse model, and further research is needed to confirm these findings in humans.
  • 2
    The mechanisms underlying the effects of miR-155 on DHA supply and neuronal survival require further investigation.
  • 3
    Further research is needed to explore the effects of miR-155 targeting transcripts encoding other factors needed for the integrity of blood-SC barrier.

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