title: Expression of neuron specific phosphatase, striatal enriched phosphatase (STEP) in reactive astrocytes after transient forebrain ischemia.
abstract: We studied the distribution and change of striatal enriched phosphatase (STEP) in the gerbil hippocampus after transient forebrain ischemia. STEP was expressed in the perikarya and in neuronal processes; it was not detected in non-neuronal cells of control animals. After 5-min forebrain ischemia, STEP immunoreactivity (STEP-IR) was preserved for 2 days; it disappeared 4 and more days after ischemia with completion of delayed neuronal death (DND) in the CA1 subfield. Furthermore, only in the CA1 after ischemia, STEP was expressed in reactive astrocytes for 4 to 28 days, showing different patterns of glial fibrillary acidic protein (GFAP)-positive reactive astrocytes. After non-or less-than lethal ischemia, STEP expression in reactive astrocytes corresponded with the degree of neuronal degeneration. Immunoblot analysis of the CA1 subfield revealed the expression of three isoforms, STEP45, -56 and -61; their expression patterns changed with time after ischemia. These data suggest that neuronal STEP is preserved until cell degeneration after ischemia and that STEP is expressed in reactive astrocytes only after lethal ischemia, with different expression patterns for its isoforms. Of STEP45, -56 and -61, STEP61 was the most strongly expressed in the reactive astrocytes; both STEP45 and -61 were expressed in neurons and the expression of STEP56 was weak. STEP may play an important role not only in neurons but also in reactive astrocytes after ischemia, depending on neuronal degeneration.
authors.affiliation: Department of Neurosurgery, Kumamoto University School of Medicine, Kumamoto, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Hasegawa
authors.forename: M
authors.initials: M
authors.lastname: Morioka
authors.forename: S
authors.initials: S
authors.lastname: Goto
authors.forename: K
authors.initials: K
authors.lastname: Korematsu
authors.forename: A
authors.initials: A
authors.lastname: Okamura
authors.forename: S
authors.initials: S
authors.lastname: Yano
authors.forename: Y
authors.initials: Y
authors.lastname: Kai
authors.forename: J I
authors.initials: JI
authors.lastname: Hamada
authors.forename: Y
authors.initials: Y
authors.lastname: Ushio
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000201:enzymology*; D015153:Blotting, Western; D002452:Cell Count; D018891:Dentate Gyrus / Q000098:blood supply / Q000201:enzymology; D004790:Enzyme Induction; D019084:Fluorescent Antibody Technique, Indirect; D005849:Gerbillinae; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D005911:Gliosis / Q000201:enzymology / Q000473:pathology; D006624:Hippocampus / Q000098:blood supply / Q000201:enzymology*; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000235:genetics; D008297:Male; D009410:Nerve Degeneration; D009419:Nerve Tissue Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D010766:Phosphorylation; D019000:Phosphotyrosine / Q000378:metabolism; D016548:Prosencephalon / Q000098:blood supply / Q000201:enzymology*; D011499:Protein Processing, Post-Translational; D017027:Protein Tyrosine Phosphatases / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D019000:Phosphotyrosine; D017027:Protein Tyrosine Phosphatases