title: Improving recovery of spinal cord-injured rats by telomerase-driven human neural progenitor cells.
abstract: OBJECTIVE
  Human neural progenitor cells hold great promise for treating a variety of human neurological diseases such as spinal cord injury. One of the issues limiting this technology is how to expand neural progenitor cells in vitro to obtain sufficient number of cells for clinical transplantation. We have established a homogeneous population of human neural progenitor cells (hNPC-TERT) immortalized by the human telomerase reverse transcriptase (hTERT) gene. Then we studied whether these cells could differentiate into neural cells in vivo and improve the recovery of spinal cord-injured rats.
  
  
  METHODS
  The hNPC-TERT cells had been transplanted into the injured spinal cord and the functional recovery of the rats with spinal cord contusion injury was evaluated through BBB locomotor scale and Motor Evoked Potentials. Additionally, the differentiation of hNPC-TERT cells was shown by immunocytochemistry.
  
  
  RESULTS
  As revealed by this animal model, hNPC-TERT cells developed into functional cells in the injured spinal cord and improved recovery from spinal cord injury in both locomotor scores and electrophysiological parameter in this animal model.
  
  
  CONCLUSIONS
  This study is the first demonstration of the use of telomerase-driven human progenitor cells to treat spinal cord injury and should provide a new cell source for research of clinical application.
authors.affiliation: Department of Orthopedics, Peking University Third Hospital, 49 West Garden Road, Beijing, 100083, P.R. China.
authors.forename: Guanghui
authors.initials: G
authors.lastname: Xu
authors.forename: Xiaoxia
authors.initials: X
authors.lastname: Li
authors.forename: Yun
authors.initials: Y
authors.lastname: Bai
authors.forename: Jinzhu
authors.initials: J
authors.lastname: Bai
authors.forename: Lingsong
authors.initials: L
authors.lastname: Li
authors.forename: Li
authors.initials: L
authors.lastname: Shen
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002478:Cells, Cultured; D004268:DNA-Binding Proteins; D004195:Disease Models, Animal; D019054:Evoked Potentials, Motor / Q000502:physiology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009043:Motor Activity / Q000502:physiology; D019081:O Antigens / Q000378:metabolism; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000502:physiology*; D009418:S100 Proteins / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000601:surgery*; D033581:Stem Cell Transplantation / Q000379:methods*; D013234:Stem Cells / Q000502:physiology*; D019098:Telomerase / Q000502:physiology*; D013997:Time Factors; D016138:Walking / Q000502:physiology*
chemical_list: D004268:DNA-Binding Proteins; D005904:Glial Fibrillary Acidic Protein; C489787:MAP2 protein, rat; D008869:Microtubule-Associated Proteins; D019081:O Antigens; D009418:S100 Proteins; C509186:TERT protein, human; D019098:Telomerase; D010751:Phosphopyruvate Hydratase