title: Mts1 protein expression in the central nervous system after injury.
abstract: We recently showed that Mts1 is expressed in white matter astrocytes in the rat brain and spinal cord from the first postnatal day. Its expression level declined in the adult CNS, but its topographical localization was maintained. Only white matter astrocytes in the cerebellum did not express Mts1. After dorsal root or sciatic nerve injury, we observed a marked upregulation of Mts1 in the area of the dorsal funiculus undergoing Wallerian degeneration. Here we show that upregulation of Mts1 is a consistent feature of astrocytes in white matter undergoing Wallerian degeneration. In addition, Mts1 is upregulated in astrocytes outlining the lesion site of a penetrating injury to the forebrain, or cerebellum. Gray matter astrocytes did not express Mts1, even after direct injury. In injured brain, we consistently noted a close relationship between Mts1-expressing astrocytes and ED1-positive microglia/macrophages, which are known to be highly motile cells. Mts1 was expressed in the periventricular area and the rostral migratory stream, i.e., sites of ongoing neuroplasticity in adulthood, and was upregulated in these areas after injury. These data suggest that Mts1-expressing astrocytes play a significant role in degenerative events in the mature white matter, interact with phagocytic microglia/macrophages and regulate cell migration and differentiation in areas of the adult brain with a high degree of plasticity.
authors.affiliation: Department of Neuroscience, Neuroanatomy, Biomedical Center, Uppsala University, Sweden. elena.kozlova@anatomi.uu.se
authors.forename: Elena N
authors.initials: EN
authors.lastname: Kozlova
authors.forename: Eugene
authors.initials: E
authors.lastname: Lukanidin
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism*; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002454:Cell Differentiation / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D002465:Cell Movement / Q000502:physiology*; D002525:Cerebellar Cortex / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D002540:Cerebral Cortex / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism*; D005260:Female; D005911:Gliosis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008264:Macrophages / Q000166:cytology / Q000378:metabolism; D017628:Microglia / Q000166:cytology / Q000378:metabolism; D009413:Nerve Fibers, Myelinated / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D013126:Spinal Nerve Roots / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology; D014855:Wallerian Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16