title: A microarray study of gene and protein regulation in human and rat brain following middle cerebral artery occlusion.
abstract: BACKGROUND
  Altered gene expression is an important feature of ischemic cerebral injury and affects proteins of many functional classes. We have used microarrays to investigate the changes in gene expression at various times after middle cerebral artery occlusion in human and rat brain.
  
  
  RESULTS
  Our results demonstrated a significant difference in the number of genes affected and the time-course of expression between the two cases. The total number of deregulated genes in the rat was 335 versus 126 in the human, while, of 393 overlapping genes between the two array sets, 184 were changed only in the rat and 36 in the human with a total of 41 genes deregulated in both cases. Interestingly, the mean fold changes were much higher in the human. The expression of novel genes, including p21-activated kinase 1 (PAK1), matrix metalloproteinase 11 (MMP11) and integrase interactor 1, was further analyzed by RT-PCR, Western blotting and immunohistochemistry. Strong neuronal staining was seen for PAK1 and MMP11.
  
  
  CONCLUSIONS
  Our findings confirmed previous studies reporting that gene expression screening can detect known and unknown transcriptional features of stroke and highlight the importance of research using human brain tissue in the search for novel therapeutic agents.
authors.affiliation: School of Biology, Chemistry and Health Science, John Dalton Building, Manchester Metropolitan University, Chester Street, Manchester, UK. n.mitsios@mmu.ac.uk
authors.forename: Nick
authors.initials: N
authors.lastname: Mitsios
authors.forename: Mohamad
authors.initials: M
authors.lastname: Saka
authors.forename: Jerzy
authors.initials: J
authors.lastname: Krupinski
authors.forename: Roberta
authors.initials: R
authors.lastname: Pennucci
authors.forename: Coral
authors.initials: C
authors.lastname: Sanfeliu
authors.forename: Qiuyu
authors.initials: Q
authors.lastname: Wang
authors.forename: Francisco
authors.initials: F
authors.lastname: Rubio
authors.forename: John
authors.initials: J
authors.lastname: Gaffney
authors.forename: Pat
authors.initials: P
authors.lastname: Kumar
authors.forename: Shant
authors.initials: S
authors.lastname: Kumar
authors.forename: Matthew
authors.initials: M
authors.lastname: Sullivan
authors.forename: Mark
authors.initials: M
authors.lastname: Slevin
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002478:Cells, Cultured; D002868:Chromosomal Proteins, Non-Histone / Q000235:genetics / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D005260:Female; D005333:Fetus; D005786:Gene Expression Regulation / Q000502:physiology*; D005947:Glucose / Q000172:deficiency; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000401:mortality; D020244:Infarction, Middle Cerebral Artery / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D008297:Male; D053507:Matrix Metalloproteinase 11 / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D000071796:SMARCB1 Protein; D020521:Stroke / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D054462:p21-Activated Kinases / Q000235:genetics / Q000378:metabolism
chemical_list: D002868:Chromosomal Proteins, Non-Histone; D004268:DNA-Binding Proteins; D000071796:SMARCB1 Protein; C513266:SMARCB1 protein, human; D014157:Transcription Factors; D054462:p21-Activated Kinases; D053507:Matrix Metalloproteinase 11; D005947:Glucose