title: Overexpression of μ-calpain in the anterior temporal neocortex of patients with intractable epilepsy correlates with clinicopathological characteristics.
abstract: OBJECTIVE
  This study aims to investigate μ-calpain expression profiles in the anterior temporal neocortex in patients with intractable epilepsy, and to determine whether its pattern of expression is related to pathological changes seen in these patients.
  
  
  METHODS
  The study subjects consisted of 30 patients with intractable epilepsy and a control group of 10 patients with brain trauma who underwent resection of the anterior temporal lobe. μ-Calpain expression in surgically resected anterior temporal cortices of patients with intractable epilepsy were analyzed using the RT-PCR, Western blot, immunohistochemistry and immunofluorescence staining. GFAP expression was detected by immunohistochemical staining. The related pro-inflammatory cytokines were quantified by elisa. Clinicopathological characteristics were evaluated by HE staining.
  
  
  RESULTS
  Analysis by Western blot and RT-PCR revealed that inactive μ-calpain expression and the calpain-cleaved spectrin fragment in surgically resected anterior temporal cortices of patients with intractable epilepsy were significantly increased compared to the tissues from corresponding regions of the control group. Immunohistological staining demonstrated that μ-calpain was overexpressed in the cell cytoplasm of neurons and glial cells in patients with intractable epilepsy and GFAP was overexpressed in the cell cytoplasm of glial cells in patients with intractable epilepsy. The level of pro-inflammatory cytokines, such as IL-1β, IL-6 and TGF-β1 were significantly increased in patients with intractable epilepsy. HE staining indicated μ-calpain overexpression is an independent prognostic factor for pathological changes such as neuronal loss, neuronal degeneration, gliosis and astrocytosis.
  
  
  CONCLUSIONS
  These data suggest that overexpression of μ-calpain is relationship with intractable epilepsy as well as the clinicopathological characteristics in these patients.
authors.affiliation: Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Neurology, Chongqing, China.
authors.forename: Zhan-hui
authors.initials: ZH
authors.lastname: Feng
authors.forename: Junwei
authors.initials: J
authors.lastname: Hao
authors.forename: Lan
authors.initials: L
authors.lastname: Ye
authors.forename: Carlos
authors.initials: C
authors.lastname: Dayao
authors.forename: Ning
authors.initials: N
authors.lastname: Yan
authors.forename: Yong
authors.initials: Y
authors.lastname: Yan
authors.forename: Lan
authors.initials: L
authors.lastname: Chu
authors.forename: Fu-dong
authors.initials: FD
authors.lastname: Shi
mesh_terms: D000293:Adolescent; D000328:Adult; D002154:Calpain / Q000096:biosynthesis* / Q000235:genetics; D004827:Epilepsy / Q000201:enzymology* / Q000473:pathology / Q000601:surgery; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006801:Humans; D007249:Inflammation / Q000201:enzymology / Q000235:genetics / Q000601:surgery; D008297:Male; D019579:Neocortex / Q000201:enzymology* / Q000473:pathology / Q000601:surgery; D013702:Temporal Lobe / Q000201:enzymology* / Q000473:pathology / Q000601:surgery; D055815:Young Adult
chemical_list: D002154:Calpain; C449002:mu-calpain