PMID- 26871686
OWN - NLM
STAT- MEDLINE
DCOM- 20161108
LR  - 20190212
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 38
IP  - 2
DP  - 2016
TI  - Bone Marrow Stromal Cells Promote Neuronal Restoration in Rats with Traumatic 
      Brain Injury: Involvement of GDNF Regulating BAD and BAX Signaling.
PG  - 748-62
LID - 10.1159/000443031 [doi]
AB  - BACKGROUND/AIMS: To investigate the effects of bone marrow stromal cells (BMSCs) 
      and underlying mechanisms in traumatic brain injury (TBI). METHODS: Cultured 
      BMSCs from green fluorescent protein-transgenic mice were isolated and confirmed. 
      Cultured BMSCs were immediately transplanted into the regions surrounding the 
      injured-brain site to test their function in rat models of TBI. Neurological 
      function was evaluated by a modified neurological severity score on the day 
      before, and on days 7 and 14 after transplantation. After 2 weeks of BMSC 
      transplantation, the brain tissue was harvested and analyzed by microarray assay. 
      And the coronal brain sections were determined by immunohistochemistry with mouse 
      anti-growth-associated protein-43 kDa (anti-GAP-43) and anti-synaptophysin to 
      test the effects of transplanted cells on the axonal regeneration in the host 
      brain. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling 
      (TUNEL) assay and Western blot were used to detect the apoptosis and expression 
      of BAX and BAD. RESULTS: Microarray analysis showed that BMSCs expressed growth 
      factors such as glial cell-line derived neurotrophic factor (GDNF). The cells 
      migrated around the injury sites in rats with TBI. BMSC grafts resulted in an 
      increased number of GAP-43-immunopositive fibers and synaptophysin-positive 
      varicosity, with suppressed apoptosis. Furthermore, BMSC transplantation 
      significantly downregulated the expression of BAX and BAD signaling. Moreover, 
      cultured BMSC transplantation significantly improved rat neurological function 
      and survival. CONCLUSION: Transplanted BMSCs could survive and improve neuronal 
      behavior in rats with TBI. Mechanisms of neuroprotection and regeneration were 
      involved, which could be associated with the GDNF regulating the apoptosis 
      signals through BAX and BAD.
CI  - (c) 2016 The Author(s) Published by S. Karger AG, Basel.
FAU - Shen, Qin
AU  - Shen Q
AD  - Institute of Neuroscience, Faculty of Basic Medicine, Kunming Medical University, 
      Kunming, China.
FAU - Yin, Yong
AU  - Yin Y
FAU - Xia, Qing-Jie
AU  - Xia QJ
FAU - Lin, Na
AU  - Lin N
FAU - Wang, You-Cui
AU  - Wang YC
FAU - Liu, Jia
AU  - Liu J
FAU - Wang, Hang-Ping
AU  - Wang HP
FAU - Lim, Apiradee
AU  - Lim A
FAU - Wang, Ting-Hua
AU  - Wang TH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160215
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 0 (bcl-Associated Death Protein)
SB  - IM
MH  - Animals
MH  - Brain/metabolism/pathology/physiopathology
MH  - Brain Injuries/*metabolism/pathology/physiopathology/*therapy
MH  - Cell Proliferation
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Glial Cell Line-Derived Neurotrophic Factor/analysis/*metabolism
MH  - *Mesenchymal Stem Cell Transplantation
MH  - Mesenchymal Stem Cells/cytology/metabolism
MH  - Mice
MH  - Mice, Transgenic
MH  - Nerve Regeneration
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - bcl-2-Associated X Protein/analysis/*metabolism
MH  - bcl-Associated Death Protein/analysis/*metabolism
EDAT- 2016/02/13 06:00
MHDA- 2016/11/09 06:00
CRDT- 2016/02/13 06:00
PHST- 2015/12/22 00:00 [accepted]
PHST- 2016/02/13 06:00 [entrez]
PHST- 2016/02/13 06:00 [pubmed]
PHST- 2016/11/09 06:00 [medline]
AID - 000443031 [pii]
AID - 10.1159/000443031 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2016;38(2):748-62. doi: 10.1159/000443031. Epub 2016 Feb 
      15.