PMID- 25218309
OWN - NLM
STAT- MEDLINE
DCOM- 20150209
LR  - 20220129
IS  - 1090-2430 (Electronic)
IS  - 0014-4886 (Linking)
VI  - 263
DP  - 2015 Jan
TI  - Increased neurotrophic factor levels in ventral mesencephalic cultures do not 
      explain the protective effect of osteopontin and the synthetic 15-mer RGD domain 
      against MPP+ toxicity.
PG  - 1-7
LID - S0014-4886(14)00288-X [pii]
LID - 10.1016/j.expneurol.2014.09.005 [doi]
AB  - The synthetic 15-mer arginine-glycine-aspartic acid (RGD) domain of osteopontin 
      (OPN) is protective in vitro and in vivo against dopaminergic cell death and this 
      protective effect may be mediated through interaction with integrin receptors to 
      regulate neurotrophic factor levels. We now examine this concept in rat primary 
      ventral mesencephalic (VM) cultures. 1-Methyl-4-phenylpyridinium (MPP+) exposure 
      reduced tyrosine hydroxylase (TH)-positive cell number and activated glial cells 
      as shown by increased glial fibrillary acidic protein (GFAP), oxycocin-42 (OX-42) 
      and ectodermal dysplasia 1 (ED-1) immunoreactivity. Both OPN and the RGD domain 
      of OPN were equally protective against MPP+ toxicity in VM cultures and both 
      increased glial-derived neurotrophic factor (GDNF) and brain-derived neurotrophic 
      factor (BDNF) levels. The effects of OPN and the RGD domain were accompanied by a 
      decrease in numbers of activated microglia but with no change in astrocyte 
      number. However, full-length OPN and the RGD domain of OPN remained protective 
      against MPP+ toxicity in the presence of a GDNF neutralising antibody. This 
      suggests that increased GDNF levels do not underlie the protective effect 
      observed with OPN. Rather, OPN's protective effect may be mediated through 
      decreased glial cell activation.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Broom, Lauren
AU  - Broom L
AD  - Neurodegenerative Diseases Research Group, Institute of Pharmaceutical Science, 
      School of Biomedical Sciences, King's College London, London, SE1 1UL, UK. 
      Electronic address: lbroom@bidmc.harvard.edu.
FAU - Jenner, Peter
AU  - Jenner P
AD  - Neurodegenerative Diseases Research Group, Institute of Pharmaceutical Science, 
      School of Biomedical Sciences, King's College London, London, SE1 1UL, UK.
FAU - Rose, Sarah
AU  - Rose S
AD  - Neurodegenerative Diseases Research Group, Institute of Pharmaceutical Science, 
      School of Biomedical Sciences, King's College London, London, SE1 1UL, UK.
LA  - eng
GR  - G-0804/PUK_/Parkinson's UK/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140916
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neurotoxins)
RN  - 0 (Oligopeptides)
RN  - 106441-73-0 (Osteopontin)
RN  - 78VO7F77PN (arginyl-glycyl-aspartic acid)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Immunohistochemistry
MH  - Mesencephalon
MH  - Nerve Growth Factors/*biosynthesis
MH  - Neuroglia/drug effects/*metabolism
MH  - Neurons/drug effects/*metabolism
MH  - Neurotoxins/toxicity
MH  - Oligopeptides/*metabolism/pharmacology
MH  - Osteopontin/*metabolism/pharmacology
MH  - Parkinsonian Disorders/metabolism
MH  - Rats
MH  - Rats, Wistar
OTO - NOTNLM
OT  - GDNF
OT  - Inflammation
OT  - Osteopontin
OT  - Parkinson's disease
OT  - Rat primary cultures
EDAT- 2014/09/15 06:00
MHDA- 2015/02/11 06:00
CRDT- 2014/09/15 06:00
PHST- 2014/06/01 00:00 [received]
PHST- 2014/09/02 00:00 [revised]
PHST- 2014/09/05 00:00 [accepted]
PHST- 2014/09/15 06:00 [entrez]
PHST- 2014/09/15 06:00 [pubmed]
PHST- 2015/02/11 06:00 [medline]
AID - S0014-4886(14)00288-X [pii]
AID - 10.1016/j.expneurol.2014.09.005 [doi]
PST - ppublish
SO  - Exp Neurol. 2015 Jan;263:1-7. doi: 10.1016/j.expneurol.2014.09.005. Epub 2014 Sep 
      16.