PMID- 18405896
OWN - NLM
STAT- MEDLINE
DCOM- 20080915
LR  - 20211027
IS  - 0014-4835 (Print)
IS  - 0014-4835 (Linking)
VI  - 86
IP  - 5
DP  - 2008 May
TI  - Expression and localisation of BDNF, NT4 and TrkB in proliferative 
      vitreoretinopathy.
PG  - 819-27
LID - 10.1016/j.exer.2008.02.010 [doi]
AB  - Exogenous brain derived neurotrophic factor (BDNF) is known to rescue ganglion 
      cell death after optic nerve injury. Its mechanism of action is believed to be 
      indirect via glial cells in the retina. In this study we investigated the changes 
      in expression and localisation of BDNF, neurotrophin-4 (NT4) and their common 
      receptor (TrkB) in retinectomy sections of patients with proliferative 
      vitreoretinopathy (PVR). Nine full-thickness retinectomy specimens obtained at 
      retinal reattachment surgery for PVR were fixed in 4% paraformaldehyde 
      immediately after excision and compared to similarly processed normal donor 
      retinas (4 eyes). Agarose-embedded sections (100 microm thick) were double 
      labelled for immunohistochemistry by confocal microscopy, with antibodies against 
      BDNF, NT4, TrkB, rod opsin, glial fibrillary acidic protein (GFAP), cellular 
      retinaldehyde binding protein (CRALBP) and Brn3. This study demonstrates 
      expression of NT4 by ganglion cells and shows expression of BDNF and NT4 in the 
      outer photoreceptor segments is downregulated during PVR, whilst NT4 is markedly 
      upregulated throughout the retina during this condition. The findings here 
      suggest that NT4 may play a neural protective role during the development of PVR. 
      It also shows that upregulation of NT4 in PVR is localised to Muller glial cells, 
      indicating either over-expression of this factor by Muller cells or that Muller 
      cells internalise NT4 for trafficking across the retina. TrkB expression was not 
      observed in PVR retina. The observations that Muller glia demonstrate 
      upregulation of NT4 suggests that retinal injury may lead to activation of this 
      neurotrophin by Muller cells as part of their neuroprotective functions.
FAU - Ghazi-Nouri, Seyed M S
AU  - Ghazi-Nouri SM
AD  - Moorfields Eye Hospital, 162 City Road, London EC1V 2PD, UK. 
      ghazinouri@hotmail.com
FAU - Ellis, James S
AU  - Ellis JS
FAU - Moss, Stephen
AU  - Moss S
FAU - Limb, G Astrid
AU  - Limb GA
FAU - Charteris, David G
AU  - Charteris DG
LA  - eng
GR  - G0300259/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080302
PL  - England
TA  - Exp Eye Res
JT  - Experimental eye research
JID - 0370707
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Eye Proteins)
RN  - 0 (Nerve Growth Factors)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Eye Proteins/*metabolism
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Nerve Growth Factors/metabolism
MH  - Receptor, trkB/metabolism
MH  - Retina/*metabolism
MH  - Retinal Ganglion Cells/metabolism
MH  - Rod Cell Outer Segment/metabolism
MH  - Vitreoretinopathy, Proliferative/*metabolism/pathology/surgery
EDAT- 2008/04/15 09:00
MHDA- 2008/09/16 09:00
CRDT- 2008/04/15 09:00
PHST- 2007/09/17 00:00 [received]
PHST- 2008/01/12 00:00 [revised]
PHST- 2008/02/26 00:00 [accepted]
PHST- 2008/04/15 09:00 [pubmed]
PHST- 2008/09/16 09:00 [medline]
PHST- 2008/04/15 09:00 [entrez]
AID - S0014-4835(08)00069-9 [pii]
AID - 10.1016/j.exer.2008.02.010 [doi]
PST - ppublish
SO  - Exp Eye Res. 2008 May;86(5):819-27. doi: 10.1016/j.exer.2008.02.010. Epub 2008 
      Mar 2.