title: Proliferation in the human ipsilateral subventricular zone after ischemic stroke.
abstract: BACKGROUND
  It is uncertain whether neurogenesis occurs in humans after stroke. We studied the morphologic changes that occurred in the subventricular zone (SVZ) in patients who died following an acute ischemic stroke.
  
  
  METHODS
  We examined coronal brain slices from patients who died after a first-ever cerebral nonlacunar infarction in the middle cerebral artery territory. We evaluated the morphologic changes in the ipsilateral and contralateral SVZ by light and electron microscopy. Using immunochemistry with Ki-67 and PCNA, we detected cell proliferation. We used Tuj-1 for immature neurons and PSA-NCAM for migrating cells.
  
  
  RESULTS
  The study included 7 patients with a mean age of 82 +/- 5 (mean +/- SD) years; 4 were men. They died a mean of 10 +/- 5 days after the ischemic stroke. Brain samples were obtained a mean of 4 +/- 2 hours after death. In comparison with the contralateral SVZ, the following changes were observed in the ipsilateral SVZ: an increase in the width of the gap and ribbon layers, as well as in the cell density of the ribbon layer, an enlargement of the cytoplasmic volume of astrocytes, and an increase of Ki-67-positive cells. In the ipsilateral SVZ, mitoses and cells that stained for either Tuj-1 or PSA-NCAM markers were observed more frequently than in the contralateral SVZ.
  
  
  CONCLUSIONS
  We found unequivocal evidence of active cell proliferation in the ipsilateral subventricular zone following an acute ischemic stroke in our patients.
authors.affiliation: Department of Neurology, Hospital de la Santa Creu i Sant Pau, Avda. Sant Antoni Maria Claret, 167, 08025 Barcelona, Spain. jmarti@santpau.cat
authors.forename: J
authors.initials: J
authors.lastname: Martí-Fàbregas
authors.forename: M
authors.initials: M
authors.lastname: Romaguera-Ros
authors.forename: U
authors.initials: U
authors.lastname: Gómez-Pinedo
authors.forename: S
authors.initials: S
authors.lastname: Martínez-Ramírez
authors.forename: E
authors.initials: E
authors.lastname: Jiménez-Xarrié
authors.forename: R
authors.initials: R
authors.lastname: Marín
authors.forename: J-L
authors.initials: JL
authors.lastname: Martí-Vilalta
authors.forename: J-M
authors.initials: JM
authors.lastname: García-Verdugo
mesh_terms: D053687:Adult Stem Cells / Q000502:physiology; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D002545:Brain Ischemia / Q000150:complications; D049109:Cell Proliferation; D002552:Cerebral Ventricles / Q000166:cytology* / Q000503:physiopathology* / Q000648:ultrastructure; D005260:Female; D007839:Functional Laterality / Q000502:physiology*; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D046529:Microscopy, Electron, Transmission / Q000379:methods; D039842:Neural Cell Adhesion Molecule L1 / Q000378:metabolism; D055495:Neurogenesis / Q000502:physiology*; D012794:Sialic Acids / Q000378:metabolism; D020521:Stroke / Q000209:etiology / Q000473:pathology*; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D019394:Ki-67 Antigen; D039842:Neural Cell Adhesion Molecule L1; D012794:Sialic Acids; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C103469:polysialyl neural cell adhesion molecule