PMID- 25744098
OWN - NLM
STAT- MEDLINE
DCOM- 20160314
LR  - 20181113
IS  - 1559-1166 (Electronic)
IS  - 0895-8696 (Linking)
VI  - 56
IP  - 2
DP  - 2015 Jun
TI  - Inhibition of miR-134 Protects Against Hydrogen Peroxide-Induced Apoptosis in 
      Retinal Ganglion Cells.
PG  - 461-71
LID - 10.1007/s12031-015-0522-9 [doi]
AB  - MicroRNAs (miRNAs) have been suggested to play an important role in neurological 
      diseases. Particularly, miR-134 is reportedly involved in regulating neuron 
      survival. However, the association between miR-134 and retinal ganglion cell 
      (RGC) survival under adverse stimulus has not been extensively investigated. In 
      this study, we aimed to explore the role and underlying mechanism of miR-134 in 
      regulating RGC apoptosis in response to hydrogen peroxide (H2O2) treatment. 
      Results showed that the expression of miR-134 dose- and time-dependently 
      increased in RGC after H2O2 treatment. H2O2-induced RGC apoptosis was 
      significantly attenuated by the inhibition of miR-134 expression by antagomiR-134 
      and was enhanced by miR-134 overexpression. Luciferase reporter assay revealed a 
      direct interaction between miR-134 and the 3'-untranslated region of cyclic 
      AMP-response element-binding protein (CREB), a critical transcription factor for 
      neuronal protection. In H2O2-treated RGCs, the inhibition of miR-134 
      significantly elevated the expression of CREB and its downstream genes, including 
      brain-derived neurotrophic factor (BDNF) and Bcl-2. Furthermore, the inhibition 
      of miR-134 also increased the expression of miR-132, a rapid response gene 
      downstream of CREB. In addition, the target gene of miR-132, acetylcholinesterase 
      was expectedly decreased by miR-134 inhibition. However, the overexpression of 
      miR-134 exerted an opposite effect. The knockdown of CREB apparently abolished 
      the protective effect of miR-134 inhibition against H2O2-induced RGC apoptosis. 
      The increased expression of BDNF and Bcl-2 induced by miR-134 inhibition was also 
      abrogated by CREB knockdown. Overall, our results suggested that the 
      downregulation of miR-134 can effectively protect against H2O2-induced RGC 
      apoptosis by negatively modulating CREB expression.
FAU - Shao, Yi
AU  - Shao Y
AD  - Department of Ophthalmology, The First Affiliated Hospital of Nanchang 
      University, No.17 Yongwaizheng Street, Donghu District, Nanchang, 330006, China.
FAU - Yu, Yao
AU  - Yu Y
FAU - Zhou, Qiong
AU  - Zhou Q
FAU - Li, Cheng
AU  - Li C
FAU - Yang, Lu
AU  - Yang L
FAU - Pei, Chong-Gang
AU  - Pei CG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150306
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (MIRN134 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (Oligonucleotides)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 3.1.1.7 (Acetylcholinesterase)
SB  - IM
MH  - Acetylcholinesterase/genetics/metabolism
MH  - Animals
MH  - *Apoptosis
MH  - Brain-Derived Neurotrophic Factor/genetics/metabolism
MH  - Cell Line
MH  - Cyclic AMP Response Element-Binding Protein/genetics/metabolism
MH  - Hydrogen Peroxide/toxicity
MH  - MicroRNAs/antagonists & inhibitors/*genetics
MH  - Oligonucleotides/pharmacology
MH  - Oxidative Stress
MH  - Rats
MH  - Retinal Ganglion Cells/*metabolism
EDAT- 2015/03/07 06:00
MHDA- 2016/03/15 06:00
CRDT- 2015/03/07 06:00
PHST- 2015/01/11 00:00 [received]
PHST- 2015/02/11 00:00 [accepted]
PHST- 2015/03/07 06:00 [entrez]
PHST- 2015/03/07 06:00 [pubmed]
PHST- 2016/03/15 06:00 [medline]
AID - 10.1007/s12031-015-0522-9 [doi]
PST - ppublish
SO  - J Mol Neurosci. 2015 Jun;56(2):461-71. doi: 10.1007/s12031-015-0522-9. Epub 2015 
      Mar 6.