title: Slowed progression in models of Huntington disease by adipose stem cell transplantation.
abstract: OBJECTIVE
  Adipose-derived stem cells (ASCs) are readily accessible and secrete multiple growth factors. Here, we show that ASC transplantation rescues the striatal pathology of Huntington disease (HD) models.
  
  
  METHODS
  ASCs were isolated from human subcutaneous adipose tissue. In a quinolinic acid (QA)-induced rat model of striatal degeneration, human ASCs (1 million cells) were transplanted into the ipsilateral striatal border immediately after the QA injection. In 60-day-old R6/2 mice transgenic for HD, ASCs (0.5 million cells) were transplanted into each bilateral striata. In in vitro experiments, we treated mutant huntingtin gene-transfected cerebral neurons with ASC-conditioned media.
  
  
  RESULTS
  In the QA model, human ASCs reduced apomorphine-induced rotation behavior, lesion volume, and striatal apoptosis. In R6/2 transgenic mice, transplantation of ASCs improved Rota-Rod performance and limb clasping, increased survival, attenuated the loss of striatal neurons, and reduced the huntingtin aggregates. ASC-transplanted R6/2 mice expressed elevated levels of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) and reactive oxygen defense enzymes and showed activation of the Akt/cAMP-response element-binding proteins. ASC-conditioned media decreased the level of N-terminal fragments of mutant huntingtin and associated apoptosis, and increased PGC-1alpha expression.
  
  
  CONCLUSIONS
  Collectively, ASC transplantation slowed striatal degeneration and behavioral deterioration of HD models, possibly via secreted factors.
authors: Department of Neurology, Clinical Research Institute, Seoul National University Hospital, Seoul, South Korea.
authors: Soon-Tae
authors: ST
authors: Lee
authors: Kon
authors: K
authors: Chu
authors: Keun-Hwa
authors: KH
authors: Jung
authors: Woo-Seok
authors: WS
authors: Im
authors: Jeong-Eun
authors: JE
authors: Park
authors: Hun-Chang
authors: HC
authors: Lim
authors: Chong-Hyun
authors: CH
authors: Won
authors: Seung-Hyun
authors: SH
authors: Shin
authors: Sang Kun
authors: SK
authors: Lee
authors: Manho
authors: M
authors: Kim
authors: Jae-Kyu
authors: JK
authors: Roh
mesh_terms: D017667:Adipocytes / Q000637:transplantation*; D000818:Animals; D045744:Cell Line, Tumor; D002478:Cells, Cultured; D003342:Corpus Striatum / Q000378:metabolism / Q000473:pathology; D017077:Culture Media, Conditioned; D004195:Disease Models, Animal; D018450:Disease Progression; D006801:Humans; D006816:Huntington Disease / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control* / Q000601:surgery*; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology; D017378:Quinolinic Acid / Q000008:administration & dosage; D051381:Rats; D017382:Reactive Oxygen Species / Q000037:antagonists & inhibitors; D033581:Stem Cell Transplantation / Q000379:methods
chemical_list: D017077:Culture Media, Conditioned; D017382:Reactive Oxygen Species; D017378:Quinolinic Acid