PMID- 25089700
OWN - NLM
STAT- MEDLINE
DCOM- 20151109
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 9
IP  - 8
DP  - 2014
TI  - Traumatic brain injury dysregulates microRNAs to modulate cell signaling in rat 
      hippocampus.
PG  - e103948
LID - 10.1371/journal.pone.0103948 [doi]
LID - e103948
AB  - Traumatic brain injury (TBI) is a common cause for cognitive and communication 
      problems, but the molecular and cellular mechanisms are not well understood. 
      Epigenetic modifications, such as microRNA (miRNA) dysregulation, may underlie 
      altered gene expression in the brain, especially hippocampus that plays a major 
      role in spatial learning and memory and is vulnerable to TBI. To advance our 
      understanding of miRNA in pathophysiological processes of TBI, we carried out a 
      time-course microarray analysis of microRNA expression profile in rat ipsilateral 
      hippocampus and examined histological changes, apoptosis and synapse 
      ultrastructure of hippocampus post moderate TBI. We found that 10 out of 156 
      reliably detected miRNAs were significantly and consistently altered from one 
      hour to seven days after injury. Bioinformatic and gene ontology analyses 
      revealed 107 putative target genes, as well as several biological processes that 
      might be initiated by those dysregulated miRNAs. Among those differentially 
      expressed microRNAs, miR-144, miR-153 and miR-340-5p were confirmed to be 
      elevated at all five time points after TBI by quantitative RT-PCR. Western blots 
      showed three of the predicated target proteins, calcium/calmodulin-dependent 
      serine protein kinase (CASK), nuclear factor erythroid 2-related factor 2 (NRF2) 
      and alpha-synuclein (SNCA), were concurrently down- regulated, suggesting that 
      miR-144, miR-153 and miR-340-5p may play important roles collaboratively in the 
      pathogenesis of TBI-induced cognitive and memory impairments. These microRNAs 
      might serve as potential targets for progress assessment and intervention against 
      TBI to mitigate secondary damage to the brain.
FAU - Liu, Liang
AU  - Liu L
AD  - Department of Forensic Medicine, Tongji Medical College of Huazhong University of 
      Science and Technology, Wuhan, China; Key Laboratory of Evidence Science, China 
      University of Political Science and Law, Ministry of Education, Beijing, China.
FAU - Sun, Tingyi
AU  - Sun T
AD  - Department of Forensic Medicine, Tongji Medical College of Huazhong University of 
      Science and Technology, Wuhan, China.
FAU - Liu, Zilong
AU  - Liu Z
AD  - Department of Forensic Medicine, Tongji Medical College of Huazhong University of 
      Science and Technology, Wuhan, China.
FAU - Chen, Xiaorui
AU  - Chen X
AD  - Department of Forensic Medicine, Tongji Medical College of Huazhong University of 
      Science and Technology, Wuhan, China.
FAU - Zhao, Lili
AU  - Zhao L
AD  - Department of Forensic Medicine, Tongji Medical College of Huazhong University of 
      Science and Technology, Wuhan, China.
FAU - Qu, Guoqiang
AU  - Qu G
AD  - Department of Forensic Medicine, Tongji Medical College of Huazhong University of 
      Science and Technology, Wuhan, China.
FAU - Li, Qingjie
AU  - Li Q
AD  - Department of Internal Medicine, The University of Texas Medical Branch at 
      Galveston, Galveston, Texas, United States of America.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140804
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (MicroRNAs)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Nfe2l2 protein, rat)
RN  - 0 (Snca protein, rat)
RN  - 0 (alpha-Synuclein)
RN  - EC 2.7.11.1 (CASK kinases)
RN  - EC 2.7.4.8 (Guanylate Kinases)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Brain Injuries/*genetics/metabolism/pathology
MH  - *Epigenesis, Genetic
MH  - Female
MH  - Gene Expression Profiling
MH  - Gene Regulatory Networks
MH  - Guanylate Kinases/genetics/metabolism
MH  - Hippocampus/injuries/*metabolism/pathology
MH  - Male
MH  - MicroRNAs/*genetics/metabolism
MH  - Molecular Sequence Annotation
MH  - NF-E2-Related Factor 2/genetics/metabolism
MH  - Oligonucleotide Array Sequence Analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction
MH  - Synapses/*genetics/metabolism/pathology/ultrastructure
MH  - Time Factors
MH  - alpha-Synuclein/genetics/metabolism
PMC - PMC4121204
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/08/05 06:00
MHDA- 2015/11/10 06:00
PMCR- 2014/08/04
CRDT- 2014/08/05 06:00
PHST- 2014/02/09 00:00 [received]
PHST- 2014/07/07 00:00 [accepted]
PHST- 2014/08/05 06:00 [entrez]
PHST- 2014/08/05 06:00 [pubmed]
PHST- 2015/11/10 06:00 [medline]
PHST- 2014/08/04 00:00 [pmc-release]
AID - PONE-D-14-05827 [pii]
AID - 10.1371/journal.pone.0103948 [doi]
PST - epublish
SO  - PLoS One. 2014 Aug 4;9(8):e103948. doi: 10.1371/journal.pone.0103948. eCollection 
      2014.