PMID- 19077183
OWN - NLM
STAT- MEDLINE
DCOM- 20090226
LR  - 20220309
IS  - 1471-2202 (Electronic)
IS  - 1471-2202 (Linking)
VI  - 9
DP  - 2008 Dec 10
TI  - Intranasal delivery of transforming growth factor-beta1 in mice after stroke 
      reduces infarct volume and increases neurogenesis in the subventricular zone.
PG  - 117
LID - 10.1186/1471-2202-9-117 [doi]
AB  - BACKGROUND: The effect of neurotrophic factors in enhancing stroke-induced 
      neurogenesis in the adult subventricular zone (SVZ) is limited by their poor 
      blood-brain barrier (BBB) permeability.Intranasal administration is a noninvasive 
      and valid method for delivery of neuropeptides into the brain, to bypass the BBB. 
      We investigated the effect of treatment with intranasal transforming growth 
      factor-beta1 (TGF-beta1) on neurogenesis in the adult mouse SVZ following focal 
      ischemia. The modified Neurological Severity Scores (NSS) test was used to 
      evaluate neurological function, and infarct volumes were determined from 
      hematoxylin-stained sections. Terminal deoxynucleotidyl transferase-mediated dUTP 
      nick end labeling (TUNEL) labeling was performed at 7 days after middle cerebral 
      artery occlusion (MCAO). Immunohistochemistry was used to detect 
      bromodeoxyuridine (BrdU) and neuron- or glia-specific markers for identifying 
      neurogenesis in the SVZ at 7, 14, 21, 28 days after MCAO. RESULTS: Intranasal 
      treatment of TGF-beta1 shows significant improvement in neurological function and 
      reduction of infarct volume compared with control animals. TGF-beta1 treated mice 
      had significantly less TUNEL-positive cells in the ipsilateral striatum than that 
      in control groups. The number of BrdU-incorporated cells in the SVZ and striatum 
      was significantly increased in the TGF-beta1 treated group compared with control 
      animals at each time point. In addition, numbers of BrdU- labeled cells 
      coexpressed with the migrating neuroblast marker doublecortin (DCX) and the 
      mature neuronal marker neuronal nuclei (NeuN) were significantly increased after 
      intranasal delivery of TGF-beta1, while only a few BrdU labeled cells co-stained 
      with glial fibrillary acidic protein (GFAP). CONCLUSION: Intranasal 
      administration of TGF-beta1 reduces infarct volume, improves functional recovery 
      and enhances neurogenesis in mice after stroke. Intranasal TGF-beta1 may have 
      therapeutic potential for cerebrovascular disorders.
FAU - Ma, Minmin
AU  - Ma M
AD  - Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, 
      305# East Zhongshan Road, Nanjing 21002, Jiangsu Province, PR China. 
      mmmxkx@gmail.com
FAU - Ma, Yuping
AU  - Ma Y
FAU - Yi, Xueming
AU  - Yi X
FAU - Guo, Ruibing
AU  - Guo R
FAU - Zhu, Wusheng
AU  - Zhu W
FAU - Fan, Xinying
AU  - Fan X
FAU - Xu, Gelin
AU  - Xu G
FAU - Frey, William H 2nd
AU  - Frey WH 2nd
FAU - Liu, Xinfeng
AU  - Liu X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081210
PL  - England
TA  - BMC Neurosci
JT  - BMC neuroscience
JID - 100966986
RN  - 0 (Dcx protein, mouse)
RN  - 0 (Doublecortin Protein)
RN  - 0 (Transforming Growth Factor beta1)
SB  - IM
MH  - *Administration, Intranasal
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Blood-Brain Barrier
MH  - Cerebrovascular Disorders/drug therapy
MH  - Corpus Striatum/physiopathology
MH  - Doublecortin Protein
MH  - Immunohistochemistry
MH  - Infarction, Middle Cerebral Artery/*drug therapy/physiopathology
MH  - Lateral Ventricles/physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurogenesis/drug effects
MH  - Recovery of Function
MH  - Transforming Growth Factor beta1/*administration & dosage/*pharmacology
PMC - PMC2637876
EDAT- 2008/12/17 09:00
MHDA- 2009/02/27 09:00
PMCR- 2008/12/10
CRDT- 2008/12/17 09:00
PHST- 2008/08/09 00:00 [received]
PHST- 2008/12/10 00:00 [accepted]
PHST- 2008/12/17 09:00 [entrez]
PHST- 2008/12/17 09:00 [pubmed]
PHST- 2009/02/27 09:00 [medline]
PHST- 2008/12/10 00:00 [pmc-release]
AID - 1471-2202-9-117 [pii]
AID - 10.1186/1471-2202-9-117 [doi]
PST - epublish
SO  - BMC Neurosci. 2008 Dec 10;9:117. doi: 10.1186/1471-2202-9-117.