An insight into new glycotherapeutics in glial inflammation: Understanding the role of glycosylation in mitochondrial function and acute to the chronic phases of inflammation

CNS Neurosci Ther, 2023 · DOI: 10.1111/cns.14016 · Published: January 1, 2023

Spinal Cord Injury Immunology Physiology

Simple Explanation

This study investigates how sugar molecules (glycans) on brain cells called astrocytes and microglia change during inflammation after a spinal cord injury. Understanding these changes could lead to new treatments. The researchers used a model of inflammation in glial cells and found that different glycans are present during the early and late stages of inflammation. They also showed that blocking certain glycan modifications can affect how mitochondria (the cell's power plants) function. The study suggests that targeting glycosylation could be a new way to treat inflammation in the brain and spinal cord. By using glycosylation inhibitors, the physiological glycosylation in mixed glial culture model cells can be replaced, which plays a role in neuroinflammation.

Study Duration

Not specified

Participants

Primary mixed glial cultures (MGCs) prepared from spinal cords of three-day-old post-natal rats

Evidence Level

Not specified

Key Findings

1
Differential glycosylation occurs in glial cells during the transition from acute to chronic inflammation in a mixed glial culture model induced by cytokines.
2
Specific N- and O-linked glycans associated with glia during spinal cord injury are differentially regulated, suggesting their involvement in the inflammatory response.
3
Inhibiting sialylation, a type of glycan modification, modulates mitochondrial function in glial cells, indicating a link between glycosylation and cellular metabolism during inflammation.

Research Summary

This study investigates the modulation of glycans in glial cells during neuroinflammation associated with spinal cord injury (SCI) using a mixed glial culture model. The researchers used lectin microarray and immunostaining to identify glycans associated with mixed glial cells and their modulation under cytokine and LPS treatments, revealing differential glycosylation patterns from acute to chronic phases of inflammation. The study also examined the effect of a sialyltransferase inhibitor (STI) on sialylation expression and mitochondrial function, suggesting that glycosylation inhibitors can replace physiological glycosylation in mixed glial culture model cells and influence neuroinflammation.

Practical Implications

Therapeutic Target Identification

Identifies glycosylation as a potential therapeutic target for neuroinflammation, paving the way for the development of glyco-therapeutics.

Biomaterial Functionalization

Suggests the use of glycosylation inhibitors for biomaterial functionalization, offering new avenues for designing biocompatible materials for neural repair.

Understanding SCI Progression

Provides a deeper understanding of the role of glycans in the progression of spinal cord injury and other neuroinflammatory conditions, potentially leading to improved diagnostic and treatment strategies.

Study Limitations

1
The study uses an in vitro model, which may not fully replicate the complexity of in vivo conditions.
2
Further research is needed to validate the findings in animal models and human clinical trials.
3
The specific mechanisms by which STI affects the NFkB pathway require further investigation.

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