title: Reduction of infarct volume and apoptosis by grafting of encapsulated basic fibroblast growth factor-secreting cells in a model of middle cerebral artery occlusion in rats.
abstract: OBJECTIVE
  This study was conducted to evaluate the effects of grafting encapsulated basic fibroblast growth factor (bFGF)-secreting cells in rat brains subjected to ischemic injury.
  
  
  METHODS
  Two cell lines were used for encapsulated grafting in this experiment, namely, a bFGF-secreting cell line established by genetic manipulation of baby hamster kidney (BHK) cells, and a naive BHK cell line. Forty-seven Sprague-Dawley rats were used in this experiment. The animals were divided into the following three groups: those receiving grafts of encapsulated bFGF-secreting cells (BHK-bFGF group); those with grafts of encapsulated naive BHK cells (naive BHK group); and those with no grafts (control group). The authors implanted encapsulated cells into the right striatum of host rats in the BHK-bFGF and naive BHK groups. Six days after grafting, the host and control animals underwent permanent right middle cerebral artery occlusion (MCAO) with an intraluminal suture procedure. The infarct volume was evaluated using 2,3,5-triphenyltetrazolium chloride staining and computerized image analysis 24 hours after MCAO. Fragmentations of DNA in the host brains were analyzed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling 12 hours after MCAO. The authors found that the infarct volume in the BHK-bFGF group was reduced by approximately 30% compared with that in the naive BHK and control groups. In the ischemic penumbral area, the number of apoptotic cells in the BHK-bFGF group was significantly decreased compared with that in the other groups.
  
  
  CONCLUSIONS
  The grafting of encapsulated BHK bFGF-secreting cells protected the brain from ischemic injury. Encapsulation and grafting of genetically engineered cells such as bFGF-secreting cells is thus thought to be a useful method for protection against cerebral ischemia.
authors.affiliation: Department of Neurological Surgery, Okayama University Medical School, Okayama City, Japan. kenjiro@gb3.so-net.ne.jp
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Fujiwara
authors.forename: Isao
authors.initials: I
authors.lastname: Date
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Shingo
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Yoshida
authors.forename: Kazuki
authors.initials: K
authors.lastname: Kobayashi
authors.forename: Akira
authors.initials: A
authors.lastname: Takeuchi
authors.forename: Akimasa
authors.initials: A
authors.lastname: Yano
authors.forename: Takashi
authors.initials: T
authors.lastname: Tamiya
authors.forename: Takashi
authors.initials: T
authors.lastname: Ohmoto
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D020520:Brain Infarction / Q000209:etiology / Q000473:pathology* / Q000517:prevention & control*; D002460:Cell Line; D017690:Cell Transplantation; D006224:Cricetinae; D004195:Disease Models, Animal; D004339:Drug Compounding; D016222:Fibroblast Growth Factor 2 / Q000008:administration & dosage* / Q000378:metabolism*; D020244:Infarction, Middle Cerebral Artery; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D014183:Transplantation, Heterologous
chemical_list: D016222:Fibroblast Growth Factor 2