PMID- 28511966
OWN - NLM
STAT- MEDLINE
DCOM- 20180531
LR  - 20240229
IS  - 1879-0267 (Electronic)
IS  - 0020-1383 (Linking)
VI  - 48
IP  - 7
DP  - 2017 Jul
TI  - Identification of potential target genes and related regulatory transcription 
      factors in spontaneous hairline fracture induced by hypervitaminosis A.
PG  - 1475-1479
LID - S0020-1383(17)30270-X [pii]
LID - 10.1016/j.injury.2017.04.042 [doi]
AB  - BACKGROUND: The aim was to research the molecular changes of bone cells induced 
      by excessive dose of vitamin A, and analyze molecular mechanism underlying 
      spontaneous fracture. METHODS: The gene expression profile of GSE29859, including 
      4 cortical bone marrow samples with excessive doses of Vitamin A and 4 control 
      cortical bone marrow samples, was obtained from the Gene Expression Omnibus (GEO) 
      database. Differentially expressed genes (DGEs) between cortical bone marrow 
      samples and control samples were screened out and pathway enrichment analysis was 
      undertaken. Based on the MSigDB database, the potential regulatory transcription 
      factors (TFs) were identified. RESULTS: A total of 373 DEGs including 342 up- and 
      31 down-regulated genes were identified. These DEGs were significantly enriched 
      in pathways of protein processing in endoplasmic reticulum, ubiquitin mediated 
      proteolysis and glycerophospholipid metabolism. Finally, the most significant 
      regulatory TFs were obtained, including E2F Transcription Factor 1 (E2F1), GA 
      Binding Protein Transcription Factor (GABP), Nuclear Factor, Erythroid 2-Like 2 
      (NRF2) and ELK1, Member of ETS Oncogene Family (ELK1). CONCLUSION: Key TFs 
      including E2F1, GABP, NRF2 and ELK1 and their targets genes such as Ube2d3, Uba1, 
      Phb2 and Tomm22 may play potential key roles in spontaneous fracture induced by 
      hypervitaminosis A. The pathways of protein processing in endoplasmic reticulum, 
      ubiquitin mediated proteolysis and glycerophospholipid metabolism may be key 
      mechanisms involved in spontaneous fracture induced by hypervitaminosis A. Our 
      findings will provide new insights for the target selection in clinical 
      application to prevent spontaneous fracture induced by hypervitaminosis A.
CI  - Copyright (c) 2017 Elsevier Ltd. All rights reserved.
FAU - Peng, Chuangang
AU  - Peng C
AD  - Orthopaedic Medical Center, The 2nd Hospital of Jilin University, Changchun, 
      Jilin 130041, China.
FAU - Yang, Qi
AU  - Yang Q
AD  - Departments of Gynecology and Obstetrics, China-Japan Union Hospital of Jilin 
      University, Changchun, Jilin 130033, China.
FAU - Wei, Bo
AU  - Wei B
AD  - Departments of Neurosurgery, China-Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130033, China.
FAU - Liu, Yong
AU  - Liu Y
AD  - Departments of Orthopaedics, Jilin Oilfield General Hospital, Songyuan 131200, 
      China.
FAU - Li, Yuxiang
AU  - Li Y
AD  - Departments of Orthopaedics, Jilin Oilfield General Hospital, Songyuan 131200, 
      China.
FAU - Gu, Dawei
AU  - Gu D
AD  - Departments of Orthopaedics, Jilin Oilfield General Hospital, Songyuan 131200, 
      China.
FAU - Yin, Guochao
AU  - Yin G
AD  - Departments of Orthopaedics, Jilin Oilfield General Hospital, Songyuan 131200, 
      China.
FAU - Wang, Bo
AU  - Wang B
AD  - Departments of Orthopaedics, Jilin Oilfield General Hospital, Songyuan 131200, 
      China.
FAU - Xu, Dehui
AU  - Xu D
AD  - Departments of Orthopaedics, Jilin Oilfield General Hospital, Songyuan 131200, 
      China.
FAU - Zhang, Xuebing
AU  - Zhang X
AD  - Departments of Orthopaedics, Jilin Oilfield General Hospital, Songyuan 131200, 
      China.
FAU - Kong, Daliang
AU  - Kong D
AD  - Departments of Orthopaedics, China-Japan Union Hospital of Jilin University, 
      Changchun, Jilin 130033, China. Electronic address: liuyongggdgg@hotmail.com.
LA  - eng
PT  - Journal Article
DEP - 20170502
PL  - Netherlands
TA  - Injury
JT  - Injury
JID - 0226040
RN  - 0 (E2f1 protein, rat)
RN  - 0 (E2F1 Transcription Factor)
RN  - 0 (Elk1 protein, rat)
RN  - 0 (ets-Domain Protein Elk-1)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Nfe2l2 protein, rat)
RN  - 0 (Transcription Factors)
RN  - 11103-57-4 (Vitamin A)
SB  - IM
MH  - Animals
MH  - Male
MH  - Rats
MH  - *Bone Marrow Cells/drug effects/metabolism
MH  - *Cortical Bone/drug effects/metabolism
MH  - E2F1 Transcription Factor/metabolism
MH  - Endoplasmic Reticulum/metabolism
MH  - Endoplasmic Reticulum Stress
MH  - ets-Domain Protein Elk-1/metabolism
MH  - *Fractures, Spontaneous/etiology/genetics
MH  - *Gene Expression Regulation/drug effects/genetics
MH  - *Hypervitaminosis A/complications/physiopathology
MH  - NF-E2-Related Factor 2/metabolism
MH  - Protein Transport
MH  - Signal Transduction
MH  - *Transcription Factors/metabolism
MH  - Transcriptome/drug effects
MH  - Vitamin A/pharmacology
OTO - NOTNLM
OT  - Pontaneous hairline fracture
OT  - Regulatory transcription factors
OT  - Target genes
OT  - Vitamin A
EDAT- 2017/05/18 06:00
MHDA- 2018/05/31 06:00
CRDT- 2017/05/18 06:00
PHST- 2016/11/16 00:00 [received]
PHST- 2017/04/06 00:00 [revised]
PHST- 2017/04/21 00:00 [accepted]
PHST- 2017/05/18 06:00 [pubmed]
PHST- 2018/05/31 06:00 [medline]
PHST- 2017/05/18 06:00 [entrez]
AID - S0020-1383(17)30270-X [pii]
AID - 10.1016/j.injury.2017.04.042 [doi]
PST - ppublish
SO  - Injury. 2017 Jul;48(7):1475-1479. doi: 10.1016/j.injury.2017.04.042. Epub 2017 
      May 2.