PMID- 20468049
OWN - NLM
STAT- MEDLINE
DCOM- 20100826
LR  - 20220330
IS  - 1098-1136 (Electronic)
IS  - 0894-1491 (Print)
IS  - 0894-1491 (Linking)
VI  - 58
IP  - 9
DP  - 2010 Jul
TI  - Astrocytic endogenous glial cell derived neurotrophic factor production is 
      enhanced by bone marrow stromal cell transplantation in the ischemic boundary 
      zone after stroke in adult rats.
PG  - 1074-81
LID - 10.1002/glia.20988 [doi]
AB  - Bone marrow stromal cells (BMSCs) facilitate functional recovery in rats after 
      focal ischemic attack. Growing evidence suggests that the secretion of various 
      bioactive factors underlies BMSCs' beneficial effects. This study investigates 
      the expression of glial cell derived neurotrophic factor (GDNF) in the ischemic 
      hemisphere with or without BMSC administration. Adult male Wistar rats were 
      subjected to 2 h of middle cerebral artery occlusion followed by an injection of 
      3 x 10(6) BMSCs (n = 11) or phosphate-buffered saline (n = 10) into the tail vein 
      24 h later. Animals were sacrificed seven days later. Single and double 
      immunohistochemical staining was performed to measure GDNF, Ki67, doublecortin, 
      and glial fibrillary acidic protein expression as well as the number of apoptotic 
      cells along the ischemic boundary zone (IBZ) and/or in the subventricular zone 
      (SVZ). BMSC treatment significantly increased GDNF expression and decreased the 
      number of apoptotic cells in the IBZ (P < 0.05). GDNF expression was colocalized 
      with GFAP. Meanwhile, BMSCs increased the number of Ki-67 positive cells and the 
      density of DCX positive migrating neuroblasts (P < 0.05). GDNF expression was 
      significantly increased in single astrocytes collected from animals treated with 
      BMSCs, and in astrocytes cocultured with BMSCs after OGD (P < 0.05). Our data 
      suggest that BMSCs increase GDNF levels in the ischemic hemisphere; the major 
      source of GDNF protein is reactive astrocytes. We propose that the increase of 
      GDNF in response to BMSC administration creates a hospitable environment for 
      local cellular repair as well as for migrating neuroblasts from the SVZ, and thus 
      contributes to the functional improvement.
CI  - Copyright 2010 Wiley-Liss, Inc.
FAU - Shen, L H
AU  - Shen LH
AD  - Department of Neurology, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, 
      Michigan 48202, USA.
FAU - Li, Y
AU  - Li Y
FAU - Chopp, M
AU  - Chopp M
LA  - eng
GR  - P01 NS042345/NS/NINDS NIH HHS/United States
GR  - R01 NS045041/NS/NINDS NIH HHS/United States
GR  - R01 NS045041-04/NS/NINDS NIH HHS/United States
GR  - R01 NS066041/NS/NINDS NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Glia
JT  - Glia
JID - 8806785
RN  - 0 (Dcx protein, rat)
RN  - 0 (Doublecortin Protein)
RN  - 0 (Gdnf protein, rat)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
SB  - IM
MH  - Aging
MH  - Animals
MH  - Apoptosis/physiology
MH  - Astrocytes/*metabolism
MH  - *Bone Marrow Transplantation
MH  - Brain/physiopathology
MH  - Brain Ischemia/physiopathology/*therapy
MH  - Doublecortin Protein
MH  - Glial Cell Line-Derived Neurotrophic Factor/*metabolism
MH  - Infarction, Middle Cerebral Artery/physiopathology/therapy
MH  - Male
MH  - Neurons/physiology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - Stem Cell Niche/physiopathology
MH  - Stroke/physiopathology/*therapy
MH  - Stromal Cells/*transplantation
PMC - PMC3096459
MID - NIHMS288320
EDAT- 2010/05/15 06:00
MHDA- 2010/08/27 06:00
PMCR- 2011/05/17
CRDT- 2010/05/15 06:00
PHST- 2010/05/15 06:00 [entrez]
PHST- 2010/05/15 06:00 [pubmed]
PHST- 2010/08/27 06:00 [medline]
PHST- 2011/05/17 00:00 [pmc-release]
AID - 10.1002/glia.20988 [doi]
PST - ppublish
SO  - Glia. 2010 Jul;58(9):1074-81. doi: 10.1002/glia.20988.