PMID- 18752297
OWN - NLM
STAT- MEDLINE
DCOM- 20090408
LR  - 20161124
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 87
IP  - 1
DP  - 2009 Jan
TI  - Glial vascular endothelial growth factor overexpression in rat brainstem under 
      tolerable hypoxia: evidence for a central chemosensitivity.
PG  - 79-85
LID - 10.1002/jnr.21837 [doi]
AB  - The ventilatory response to hypoxia is mediated by peripheral inputs arising from 
      the arterial chemoreceptors. In their absence, hypoxic adaptation can be 
      achieved, possibly as a result of central cellular reorganization. To study this 
      reorganization, we used chemodenervated rats to investigate the expression and 
      localization of vascular endothelial growth factor (VEGF) in the brainstem. VEGF 
      is a target gene of hypoxia-inducible factor (HIF) that is responsible for the 
      morphofunctional remodeling induced by hypoxia. Intact and chemodenervated rats 
      were subjected to normoxia or hypoxia for 6 hr (10% O(2) in N(2)). VEGF protein 
      was quantified in micropunches of brainstem tissue. Only chemodenervated animals 
      showed an increased VEGF expression in response to hypoxia, whereas, in normoxia, 
      VEGF expression was not modified by chemodenervation. The same hypoxic condition 
      was repeated for 8 days before immunocytochemical staining with anti-VEGF; 
      antiglial fibrillary acidic protein (GFAP), a marker of astrocytes; and anti-rat 
      endothelial cell antigen-1 (anti-RECA-1) that recognizes endothelial cells. 
      Confocal analysis showed a cellular colocalization of GFAP and VEGF, indicating 
      that VEGF was overexpressed predominantly in astrocytes. Increased RECA-1 
      immunolabeling indicated an enhanced angiogenesis in chemodenervated rats 
      subjected to hypoxia. These results indicate that glial cells and the vascular 
      network contribute to the brainstem remodeling. The peripheral chemodenervation 
      reveals a central O(2) chemosensitivity involving a cascade of gene expression 
      triggered by hypoxia, which in intact animals may act synergically with 
      peripheral chemosensory inputs.
CI  - 2008 Wiley-Liss, Inc.
FAU - Perrin, J S
AU  - Perrin JS
AD  - Universite de Lyon, Lyon, France.
FAU - Araneda, S
AU  - Araneda S
FAU - Catteau, J
AU  - Catteau J
FAU - Autran, S
AU  - Autran S
FAU - Denavit-Saubie, M
AU  - Denavit-Saubie M
FAU - Pequignot, J M
AU  - Pequignot JM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Antigens, Surface)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (endothelial cell-monocyte antigens)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Antigens, Surface/metabolism
MH  - Brain Stem/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay/methods
MH  - Gene Expression Regulation/*physiology
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Glossopharyngeal Nerve/physiopathology
MH  - Glossopharyngeal Nerve Injuries
MH  - Hypoxia/*pathology
MH  - Male
MH  - Membrane Glycoproteins/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Rhizotomy/methods
MH  - Statistics, Nonparametric
MH  - Vascular Endothelial Growth Factor A/*metabolism
EDAT- 2008/08/30 09:00
MHDA- 2009/04/09 09:00
CRDT- 2008/08/30 09:00
PHST- 2008/08/30 09:00 [entrez]
PHST- 2008/08/30 09:00 [pubmed]
PHST- 2009/04/09 09:00 [medline]
AID - 10.1002/jnr.21837 [doi]
PST - ppublish
SO  - J Neurosci Res. 2009 Jan;87(1):79-85. doi: 10.1002/jnr.21837.