PMID- 28933219
OWN - NLM
STAT- MEDLINE
DCOM- 20180514
LR  - 20191210
IS  - 1555-3892 (Electronic)
IS  - 0963-6897 (Print)
IS  - 0963-6897 (Linking)
VI  - 26
IP  - 7
DP  - 2017 Jul
TI  - Suppression of Trim32 Enhances Motor Function Repair after Traumatic Brain Injury 
      Associated with Antiapoptosis.
PG  - 1276-1285
LID - 10.1177/0963689717716510 [doi]
AB  - To investigate the role of Trim32 in traumatic brain injury (TBI), adult male 
      Sprague Dawley (SD) rats and mice were randomly divided into sham (n = 6) and TBI 
      groups ( n = 24), respectively. Then, mice were assigned into Trim32 knockout 
      mice (Trim32-KO [+/-]) and wild-type (WT) littermates. The TBI model used was the 
      Feeney free-falling model, and neurological function was evaluated after TBI 
      using a neurological severity score (NSS). Reverse transcription polymerase chain 
      reaction (RT-PCR), Western blot, and immunohistochemistry were used to 
      investigate the expression of Trim32 in the damaged cortex. Cell apoptosis in the 
      cortex was detected by terminal-deoxynucleoitidyl transferase-mediated dUTP nick 
      end labeling (TUNEL) staining. Moreover, Trim32-KO (+/-) mice were used to 
      determine the effect of Trim in neurological repair after TBI. Results showed the 
      NSS scores in TBI rats were significantly increased from day 1 to day 11 
      postoperation, compared with the sham group. Trim32 messenger RNA (mRNA) 
      expression in the cortex was significantly increased at 7 d after TBI, while the 
      level of Tnr and cytochrome c oxidase polypeptide 5A mRNA didn't exhibit 
      significant changes. In addition, Western blot was used to detect the level of 
      Trim32 protein in the cortex. Trim32 expression was significantly increased at 7 
      d after TBI, and immunoreactive Trim32-positive cells were mainly neurons. 
      Moreover, Trim32-KO (+/-) mice with TBI had lower NSS scores than those in the WT 
      group from day 1 to day 11 postoperation. Meanwhile, Trim32-KO (+/-) mice had a 
      decreased number of TUNEL-positive cells compared with the control group at 3 d 
      postoperation. Protein 73 (p73) decreased at 7 d postoperation in Trim32-KO (+/-) 
      mice with TBI, when compared with WT mice with TBI. Our study is the first to 
      confirm that suppression of Trim32 promotes the recovery of neurological function 
      after TBI and to demonstrate that the underlying mechanism is associated with 
      antiapoptosis, which may be associated with p73.
FAU - Zhang, Zi-Bin
AU  - Zhang ZB
AD  - 1 Institute of Neurological Disease, Department of Anesthesiology, Translational 
      Neuroscience Center, West China Hospital, Sichuan University, Chengdu, China.
FAU - Xiong, Liu-Lin
AU  - Xiong LL
AD  - 1 Institute of Neurological Disease, Department of Anesthesiology, Translational 
      Neuroscience Center, West China Hospital, Sichuan University, Chengdu, China.
FAU - Lu, Bin-Tuan
AU  - Lu BT
AD  - 2 Institute of Neuroscience, Kunming Medical University, Kunming, China.
FAU - Zhang, Hui-Xiang
AU  - Zhang HX
AD  - 2 Institute of Neuroscience, Kunming Medical University, Kunming, China.
FAU - Zhang, Piao
AU  - Zhang P
AD  - 2 Institute of Neuroscience, Kunming Medical University, Kunming, China.
FAU - Wang, Ting-Hua
AU  - Wang TH
AD  - 1 Institute of Neurological Disease, Department of Anesthesiology, Translational 
      Neuroscience Center, West China Hospital, Sichuan University, Chengdu, China.
AD  - 2 Institute of Neuroscience, Kunming Medical University, Kunming, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cell Transplant
JT  - Cell transplantation
JID - 9208854
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (NeuN protein, mouse)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Transcription Factors)
RN  - 0 (Tripartite Motif Proteins)
RN  - 0 (Trp73 protein, mouse)
RN  - 0 (Tumor Protein p73)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
RN  - EC 2.3.2.27 (TRIM32 protein, mouse)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.3.2.27 (trim32 protein, rat)
SB  - IM
MH  - Animals
MH  - *Apoptosis/genetics
MH  - Behavior, Animal
MH  - Brain Injuries, Traumatic/genetics/*pathology/*physiopathology
MH  - DNA-Binding Proteins
MH  - Disease Models, Animal
MH  - Electron Transport Complex IV/metabolism
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Mice, Knockout
MH  - *Motor Activity
MH  - *Nerve Regeneration
MH  - Nerve Tissue Proteins/metabolism
MH  - Nuclear Proteins/metabolism
MH  - Rats, Sprague-Dawley
MH  - Transcription Factors/genetics/*metabolism
MH  - Tripartite Motif Proteins/genetics/*metabolism
MH  - Tumor Protein p73/metabolism
MH  - Ubiquitin-Protein Ligases/genetics/*metabolism
MH  - Up-Regulation/genetics
PMC - PMC5657740
OTO - NOTNLM
OT  - Trim32
OT  - antiapoptosis
OT  - motor function
OT  - traumatic brain injury
COIS- Declaration of Conflicting Interests: The author(s) declared no potential 
      conflicts of interest with respect to the research, authorship, and/or 
      publication of this article.
EDAT- 2017/09/22 06:00
MHDA- 2018/05/15 06:00
PMCR- 2017/07/01
CRDT- 2017/09/22 06:00
PHST- 2017/09/22 06:00 [entrez]
PHST- 2017/09/22 06:00 [pubmed]
PHST- 2018/05/15 06:00 [medline]
PHST- 2017/07/01 00:00 [pmc-release]
AID - 10.1177_0963689717716510 [pii]
AID - 10.1177/0963689717716510 [doi]
PST - ppublish
SO  - Cell Transplant. 2017 Jul;26(7):1276-1285. doi: 10.1177/0963689717716510.