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Midkine in repair of the injured nervous system
Yoshihiro Yoshida1, Harutoshi Sakakima, Fumiyo Matsuda
1School of Health Sciences, Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
Unlabelled:
Midkine (MK) is a growth factor with neurotrophic and neurite outgrowth activities. It was expressed in the peri-ischaemic area in the acute phase of cerebral infarction in rat brains. Astrocytes were the origin of MK in this occasion. MK has been assessed in terms of its effects on neural injury. The administration of MK into the lateral ventricle immediately prior to ischaemia prevented cell death in the hippocampal CA1 neurons degenerated by transient forebrain ischaemia in gerbils. MK administration was also beneficial in rats with neural injury, especially after kainic acid-induced seizures. Gene therapy with mouse MK cDNA using an adenovirus was effective in reducing the cerebral infarction volume and in increasing the number of neuronal precursor cells in the subventricular zone of the rat brain. MK mRNA and MK protein were found in spinal cord motor neurons of the anterior horn in both the acute phase of sciatic nerve injury and 3 weeks later. MK immunoreactivity was also found in the proximal side of a sciatic nerve-injured site in sciatic nerve axons. MK receptors were expressed in Schwann cells after injury, suggesting crosstalk between axons and Schwann cells. MK was also present in nerve terminals and influenced ACh receptor clustering during neuromuscular development in Xenopus. Thus, MK may also be involved in reinforcing and maintaining the synapse. All these findings indicate the therapeutic potential of MK for promoting repair of the nervous system after injury.
Linked Articles:
This article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-4.
Insights
Midkine (MK), a growth factor, shows therapeutic potential for nervous system repair. Studies demonstrate MK protects neurons from injury and aids in recovery after brain and spinal cord damage.
Area of Science:
- Neuroscience
- Molecular Biology
- Regenerative Medicine
Background:
- Midkine (MK) is a growth factor known for its neurotrophic and neurite outgrowth properties.
- MK is expressed in brain tissue following cerebral infarction, with astrocytes identified as its source.
- The role of MK in neural injury and repair has been a focus of recent research.
Purpose of the Study:
- To investigate the therapeutic potential of Midkine (MK) in various models of nervous system injury.
- To explore the effects of MK administration and gene therapy on neuronal survival and tissue repair.
- To examine the expression and localization of MK and its receptors in response to nerve injury.
Main Methods:
- Administration of MK into the lateral ventricle prior to ischemic events in gerbils and rats.
- Induction of neural injury using kainic acid in rats.
- Gene therapy utilizing adenovirus-mediated delivery of mouse MK cDNA.
- Analysis of MK mRNA and protein expression in spinal cord motor neurons and sciatic nerve axons post-injury.
- Investigation of MK receptor expression in Schwann cells.
Main Results:
- MK administration protected hippocampal CA1 neurons from cell death following transient forebrain ischemia.
- MK proved beneficial in rats with kainic acid-induced seizures and other neural injuries.
- Adenovirus-mediated MK gene therapy reduced cerebral infarction volume and increased neuronal precursor cells.
- MK was detected in spinal cord motor neurons and sciatic nerve axons after injury, with receptors expressed on Schwann cells.
- MK influenced acetylcholine receptor clustering during neuromuscular development.
Conclusions:
- Midkine (MK) demonstrates significant neuroprotective and regenerative capabilities across different models of central and peripheral nervous system injury.
- MK plays a role in axonal-Schwann cell interactions and synaptic maintenance.
- These findings highlight MK as a promising therapeutic agent for promoting nervous system repair and recovery.
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