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Alteration of midkine expression in the ischemic brain of humans
Manabu Wada1, Makiko Kamata, Yoshinori Aizu
1Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan.
Abstract:
Midkine (MK) is a heparin-binding growth factor that occurs as a product of the retinoic acid-inducible gene. Alteration of MK expression in ischemic brain lesions was examined in humans immunohistochemically in nine patients and in two control subjects without neurological disorders. Some neurons were MK-immunopositive, but no evident MK-immunoreactivity was observed in astrocytes in brains of control subjects. In the ischemic lesions, significant elevation of MK-immunoreactivity in the astrocytes and depletion of the reactivity in neurons were seen, especially in the early period, where edema and eosinophilic neurons were prominent. On the other hand, MK-immunoreactivity was not observed in hypertrophic and fibrillary astrocytes in the later period. These findings suggest that the MK in astrocytes play some role in the repair process in the early period of the ischemic brain lesions in humans.
Insights
Midkine (MK) is a growth factor. In human ischemic brain lesions, MK levels increase in astrocytes during early stages, suggesting a role in brain repair.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Midkine (MK) is a heparin-binding growth factor encoded by a retinoic acid-inducible gene.
- MK is implicated in various biological processes, including cell growth, differentiation, and tissue repair.
Purpose of the Study:
- To investigate the alteration of Midkine (MK) expression in human ischemic brain lesions.
- To determine the cellular localization and temporal changes of MK in the context of brain ischemia.
Main Methods:
- Immunohistochemical analysis of brain tissue samples from nine human patients with ischemic lesions and two control subjects.
- Assessment of MK-immunoreactivity in neurons and astrocytes at different stages of ischemic injury.
Main Results:
- Control brains showed MK-immunopositive neurons but no reactivity in astrocytes.
- Ischemic lesions exhibited significantly elevated MK-immunoreactivity in astrocytes and decreased reactivity in neurons, particularly in the early phase characterized by edema and eosinophilic neurons.
- MK-immunoreactivity was absent in hypertrophic and fibrillary astrocytes during the later stages of lesion development.
Conclusions:
- Astrocytic Midkine (MK) expression is significantly altered in human ischemic brain lesions.
- The findings suggest that MK in astrocytes plays a crucial role in the early repair processes following ischemic brain injury.
- The dynamic changes in MK localization indicate a complex involvement in the response to neuronal damage.