PMID- 23973300
OWN - NLM
STAT- MEDLINE
DCOM- 20140508
LR  - 20131007
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 553
DP  - 2013 Oct 11
TI  - MicroRNA profiling and the role of microRNA-132 in neurodegeneration using a rat 
      model.
PG  - 153-8
LID - S0304-3940(13)00720-9 [pii]
LID - 10.1016/j.neulet.2013.08.001 [doi]
AB  - MicroRNAs (miRs) are endogenous small RNAs that regulate gene expression at the 
      post-transcriptional level by mediating mRNA degradation or transcriptional 
      inhibition. MiRs were implicated in the pathogenesis of numerous 
      neurodegenerative diseases, including Parkinson's disease (PD). In this study we 
      analyzed the possible role of miRs in the neurodegenerative process in a 
      spontaneous autosomal recessive rat model for neurodegeneration developed in our 
      laboratory. To investigate the role of miRs in the etiology of PD, we conducted 
      miR expression profiling using microarrays. We found 20 miRs that are deregulated 
      in affected rats and many of these are implicated in neurodegenerative disease, 
      including PD. In this study we were particularly interested in the expression of 
      miR-132, a miR that has been reported to be highly expressed in neurons, and to 
      have a potential role in neurodegenerative diseases. We found a significant 
      increase in miR-132 in affected rats by microarray and the result was confirmed 
      by qPCR. Next we analyzed one of the known downstream targets of miR-132, nuclear 
      receptor related 1 protein (Nurr1), which is essential in neurogenesis of 
      midbrain dopaminergic neurons. Western blot analysis and immunohistochemistry 
      revealed a significant decrease in Nurr1 protein expression in the mesencephalic 
      neurons. Finally, we found a significant decrease in both serum and mesencephalon 
      brain tissue of brain-derived neurotrophic factor (BDNF), which is known to be a 
      direct target of Nurr1. Taken together, our findings suggest that miR-132 can 
      regulate Nurr1 levels and might influence the development and function of 
      midbrain dopaminergic neurons.
CI  - Copyright (c) 2013 Elsevier Ireland Ltd. All rights reserved.
FAU - Lungu, Gina
AU  - Lungu G
AD  - Department of Veterinary Pathobiology, Texas A&M University, College Station, TX 
      77843, USA.
FAU - Stoica, George
AU  - Stoica G
FAU - Ambrus, Andy
AU  - Ambrus A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130821
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (MIRN132 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (Nr4a2 protein, rat)
RN  - 0 (Nuclear Receptor Subfamily 4, Group A, Member 2)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Disease Models, Animal
MH  - Gene Expression Profiling
MH  - Gene Expression Regulation
MH  - Mesencephalon/metabolism
MH  - MicroRNAs/*metabolism
MH  - Nerve Degeneration/*metabolism
MH  - Nuclear Receptor Subfamily 4, Group A, Member 2/metabolism
MH  - Rats
OTO - NOTNLM
OT  - BDNF
OT  - MicroRNA
OT  - MicroRNA-132
OT  - Neurodegeneration
OT  - Nurr1
OT  - Rat model
EDAT- 2013/08/27 06:00
MHDA- 2014/05/09 06:00
CRDT- 2013/08/27 06:00
PHST- 2013/05/20 00:00 [received]
PHST- 2013/07/19 00:00 [revised]
PHST- 2013/08/02 00:00 [accepted]
PHST- 2013/08/27 06:00 [entrez]
PHST- 2013/08/27 06:00 [pubmed]
PHST- 2014/05/09 06:00 [medline]
AID - S0304-3940(13)00720-9 [pii]
AID - 10.1016/j.neulet.2013.08.001 [doi]
PST - ppublish
SO  - Neurosci Lett. 2013 Oct 11;553:153-8. doi: 10.1016/j.neulet.2013.08.001. Epub 
      2013 Aug 21.