Journal of the Neurological Sciences
Volume 200, Issue 1 , Pages 67-73, 15 August 2002

Alteration of midkine expression in the ischemic brain of humans

  • Manabu Wada

      Affiliations

    • Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan
    • Third Department of Internal Medicine, Yamagata University, Yamagata 990-9585, Japan
    • Department of Neurology, Tokyo Metropolitan Neurological Hospital, Tokyo 183-0042, Japan
  • ,
  • Makiko Kamata

      Affiliations

    • Section of Biosignals, R&D Center, BML, Saitama 350-1101, Japan
  • ,
  • Yoshinori Aizu

      Affiliations

    • Section of Biosignals, R&D Center, BML, Saitama 350-1101, Japan
  • ,
  • Takashi Morita

      Affiliations

    • Department of Pathology, Shinrakuen Hospital, Niigata 950-2087, Japan
  • ,
  • Jianguo Hu

      Affiliations

    • Section of Biosignals, R&D Center, BML, Saitama 350-1101, Japan
    • Present address: Fuji Photo Optical Co. LTD, Saitama 330-8624, Japan.
  • ,
  • Kiyomitsu Oyanagi

      Affiliations

    • Corresponding Author InformationCorresponding author. Tel.: +81-42-325-3881x4711; fax: +81-42-321-8678
    • Department of Neuropathology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan

Received 28 November 2001; received in revised form 25 March 2002; accepted 9 May 2002.

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.

Keywords:  Astrocyte, Cerebral infarct, Glial fibrillary acidic protein, Human, Midkine

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PII: S0022-510X(02)00134-X

Journal of the Neurological Sciences
Volume 200, Issue 1 , Pages 67-73, 15 August 2002