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Midkine exists in astrocytes in the early stage of cerebral infarction

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Abstract

Midkine (MK), a heparin-binding neurotrophic factor, is expressed in the early stage of experimental cerebral infarction in the zone surrounding the infarct. Double immunostaining with anti-MK and anti-glial fibrillary acidic protein showed existence of MK in astrocytic cytoplasm on postoperative day 2. Immunoelectron microscopic analysis revealed the presence of MK in the swollen astrocytic processes on postoperative day 4. Thus, MK was localized in astrocytes upon cerebral infarction.

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    Differences in the temporal regulation of PTN and MK in situations of brain damage could underlie the differential modulation of amphetamine-induced neurotoxicity by endogenous PTN and MK. Both PTN and MK are usually upregulated in astrocytes after nerve injury (Takeda et al., 1995; Wang et al., 1998; Mochizuki et al., 1998; Yeh et al., 1998; Kim et al., 2010). However, the temporal regulation of expression of both cytokines differs.

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    Gene knockout mice deficient in MK showed retarded postnatal development in the hippocampus [20]. Following experimental cerebral infarction in rats, MK expression is intensely induced in the surrounding edematic region, but not in the necrotic region, shortly after infarction [32,34]. Its expression is also increased in the hippocampal CA1 subfield following transient forebrain ischemia in rats [17].

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