title: Traumatic injury-induced midkine expression in the adult rat spinal cord during the early stage.
abstract: Spinal cord injury is a debilitating condition. Midkine (MK) is involved in the generation of the central nervous system during development; however, the role of MK in the mature spinal cord has not been clarified. We examined the expression of MK, which has neurotrophic activity, before and after traumatic injury to the adult rat spinal cord. Following laminectomy, the rat spinal cord was injured at the T-9 level by applying extradural static weight-compression, in which a cylindrical compressor was used to induce complete and irreversible transverse spinal cord injury with paralysis of the lower extremities. The expression of MK was examined up to 14 days after the injury by immunohistochemical and Western blot analyses. Intense MK immunoreactivity was observed in the gray matter around the injury site but not in the necrotic lesion 1-7 days postinjury, although it was slightly positive 14 days after the injury. MK immunoreactivity was not detected in the normal spinal cord. The expression of MK was an early event, and its expression was compared to the increased production of glial fibrillary acidic protein (GFAP), a marker of reactive astrocytes, that was elevated at 2 days postinjury and continued over a 14 day period following the injury. Double immunostaining with anti-MK and anti-GFAP showed the existence of MK in the astrocytic cytoplasm. These findings suggest that MK was produced in astrocytes approximating the damaged region and may represent a reparative neurotrophic factor during the early phase of traumatic injury of the spinal cord.
authors.affiliation: School of Medical Sciences, Faculty of Medicine, Kagoshima University, Kagoshima, Japan. sakaki@health.nop.kagoshima-u.ac.jp
authors.forename: Harutoshi
authors.initials: H
authors.lastname: Sakakima
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Takashi
authors.initials: T
authors.lastname: Muramatsu
authors.forename: Kazunori
authors.initials: K
authors.lastname: Yone
authors.forename: Masamichi
authors.initials: M
authors.lastname: Goto
authors.forename: Kosei
authors.initials: K
authors.lastname: Ijiri
authors.forename: Shuji
authors.initials: S
authors.lastname: Izumo
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism*; D016207:Cytokines; D004195:Disease Models, Animal; D018450:Disease Progression; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D000078792:Midkine; D009414:Nerve Growth Factors / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000502:physiology; D020127:Recovery of Function / Q000502:physiology; D013116:Spinal Cord / Q000254:growth & development*; D013119:Spinal Cord Injuries / Q000503:physiopathology* / Q000628:therapy
chemical_list: D002352:Carrier Proteins; D016207:Cytokines; D005904:Glial Fibrillary Acidic Protein; D009414:Nerve Growth Factors; D000078792:Midkine