title: Heat shock protein-27 is upregulated in the temporal cortex of patients with epilepsy.
abstract: OBJECTIVE
  Heat shock protein-27 (HSP-27) belongs to the group of small heat shock proteins that become induced in response to various pathologic conditions. HSP-27 has been shown to protect cells and subcellular structures, particularly mitochondria, and serves as a carrier for estradiol. It is a reliable marker for tissues affected by oxidative stress. Oxidative stress and related cellular defence mechanisms are currently thought to play a major role during experimentally induced epileptic neuropathology. We addressed the question whether HSP-27 becomes induced in the neocortex resected from patients with pharmacoresistant epilepsy.
  
  
  METHODS
  Human epileptic temporal neocortex was obtained during neurosurgery, and control tissue was obtained at autopsy from subjects without known neurologic diseases. The tissues were either frozen for Western blot analysis or fixed in Zamboni's fixative for the topographic detection of HSP-27 at the cellular level by means of immunohistochemistry.
  
  
  RESULTS
  HSP-27 was highly expressed in all epilepsy specimens and in the cortex of a patient who died in the final stage of multiple sclerosis (positive control), whereas only low amounts of HSP-27 were detectable in control brains. In epilepsy patients, HSP-27 was present in astrocytes and in the walls of blood vessels. The intracortical distribution patterns varied strongly among the epilepsy specimens.
  
  
  CONCLUSIONS
  These results demonstrate that HSP-27 becomes induced in response to epileptic pathology. Although the functional aspects of HSP-27 induction during human epilepsy have yet to be elucidated, it can be concluded that HSP-27 is a marker for cortical regions in which a stress response has been caused by seizures.
authors.affiliation: C. & O. Vogt Institute for Brain Research, Dusseldorf, Germany.
authors.forename: Hans-J
authors.initials: HJ
authors.lastname: Bidmon
authors.forename: Boris
authors.initials: B
authors.lastname: Görg
authors.forename: Nicola
authors.initials: N
authors.lastname: Palomero-Gallagher
authors.forename: Friedrich
authors.initials: F
authors.lastname: Behne
authors.forename: Rainer
authors.initials: R
authors.lastname: Lahl
authors.forename: Hans W
authors.initials: HW
authors.lastname: Pannek
authors.forename: Erwin-J
authors.initials: EJ
authors.lastname: Speckmann
authors.forename: Karl
authors.initials: K
authors.lastname: Zilles
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001253:Astrocytes / Q000737:chemistry / Q000378:metabolism; D015415:Biomarkers; D001812:Blood-Brain Barrier / Q000378:metabolism; D015153:Blotting, Western; D002675:Child, Preschool; D004827:Epilepsy / Q000175:diagnosis / Q000378:metabolism* / Q000601:surgery; D005260:Female; D055551:HSP27 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000032:analysis / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D018832:Molecular Chaperones; D019579:Neocortex / Q000737:chemistry / Q000378:metabolism; D009363:Neoplasm Proteins / Q000032:analysis / Q000378:metabolism; D013702:Temporal Lobe / Q000737:chemistry* / Q000378:metabolism / Q000601:surgery; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D055551:HSP27 Heat-Shock Proteins; C057725:HSPB1 protein, human; D006360:Heat-Shock Proteins; D018832:Molecular Chaperones; D009363:Neoplasm Proteins