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  4. C-X-C chemokine receptor type 7 antibody enhances neural plasticity after ischemic stroke

C-X-C chemokine receptor type 7 antibody enhances neural plasticity after ischemic stroke

NEURAL REGENERATION RESEARCH, 2023 · DOI: https://doi.org/10.4103/1673-5374.363835 · Published: January 5, 2023

Regenerative MedicineNeurology

Simple Explanation

This study investigates the role of CXCR7, a receptor, in neural regeneration after stroke in rats. By injecting a CXCR7-neutralizing antibody, the researchers aimed to block the interaction between SDF-1 and CXCR7 to observe the effects on axonal regeneration, synaptogenesis, remyelination, and motor function recovery. The results showed that blocking CXCR7 with the antibody led to increased growth of nerve fibers, enhanced synapse formation in the spinal cord, and improved myelin regeneration in the brain. These changes suggest that CXCR7 influences neural plasticity after stroke. Furthermore, the study found that the beneficial effects of the CXCR7 antibody might be related to the activation of the CXCR4 receptor and the RAS/ERK signaling pathway, indicating a potential therapeutic target for stroke recovery.

Study Duration
Not specified
Participants
52 male Wistar rats
Evidence Level
Not specified

Key Findings

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    CXCR7-neutralizing antibody increased the total length and number of sprouting corticospinal tract fibers in rats with cerebral ischemia, indicating enhanced axonal regeneration.
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    CXCR7 antibody treatment significantly increased vGlut1 and GAP43 expression levels in the ischemic rats, suggesting enhanced synaptogenesis after cerebral ischemia.
  • 3
    Anti-CXCR7 antibody treatment not only significantly upregulated the proportion of Olig2+BrdU+ cells but also greatly increased the MBP expression level in both ischemic rats and sham-operated rats, indicating augmented differentiation and maturation of OPCs.

Research Summary

This study investigates the effect of CXCR7 antibody on neural plasticity after ischemic stroke in rats. The researchers found that CXCR7 antibody increased axonal regeneration, synaptogenesis and myelin regeneration. The study also revealed that CXCR7 antibody upregulated SDF-1 and CXCR4 expression and activated the RAS/ERK signaling pathway after cerebral ischemia. These molecular changes may contribute to the observed improvements in neural plasticity. The findings suggest that inhibition of CXCR7 may provide a promising new therapeutic target for neural plasticity and neurological functional recovery in the chronic stage of stroke.

Practical Implications

Therapeutic Target

Inhibition of CXCR7 may represent a novel therapeutic strategy for promoting neural plasticity and functional recovery after stroke.

RAS/ERK pathway activation

Activating the RAS/ERK signaling pathway, potentially through CXCR4, could be a mechanism to enhance recovery after ischemic brain injury.

Remyelination Enhancement

Targeting CXCR7 could facilitate remyelination, contributing to improved outcomes following white matter injury induced by stroke.

Study Limitations

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