PMID- 27665569
OWN - NLM
STAT- MEDLINE
DCOM- 20170328
LR  - 20181113
IS  - 1559-1166 (Electronic)
IS  - 0895-8696 (Linking)
VI  - 61
IP  - 1
DP  - 2017 Jan
TI  - Oxygen-Glucose Deprivation Induces G2/M Cell Cycle Arrest in Brain Pericytes 
      Associated with ERK Inactivation.
PG  - 105-114
LID - 10.1007/s12031-016-0844-2 [doi]
AB  - Growing evidence has revealed that brain pericytes are multifunctional and 
      contribute to the pathogenesis of a number of neurological disorders. However, 
      the role of pericytes in cerebral ischemia, and especially the pathophysiological 
      alterations in pericytes, remains unclear. In the present study, our aim was to 
      determine whether the proliferation of pericytes is affected by cerebral ischemia 
      and, if so, to identify the underlying mechanism(s). Cultured brain pericytes 
      subjected to oxygen-glucose deprivation (OGD) were used as our model of cerebral 
      ischemia; the protein expression levels of cyclin D1, cyclin E, cdk4, and cyclin 
      B1 were determined by Western blot analysis, and cell cycle analysis was assessed 
      by flow cytometry. The OGD treatment reduced the brain pericyte proliferation by 
      causing G2/M phase arrest and downregulating the protein levels of cyclin D1, 
      cyclin E, cdk4, and cyclin B1. Further studies demonstrated a simultaneous 
      decrease in the activity of extracellular regulated protein kinases (ERK), 
      suggesting a critical role of the ERK signaling cascade in the inhibition of 
      OGD-induced pericyte proliferation. We suggest that OGD inhibition of the 
      proliferation of brain pericytes is associated with the inactivation of the ERK 
      signaling pathway, which arrests them in the G2/M phase.
FAU - Wei, Wenjie
AU  - Wei W
AD  - Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, People's Republic of China.
FAU - Yu, Zhiyuan
AU  - Yu Z
AD  - Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, People's Republic of China.
FAU - Xie, Minjie
AU  - Xie M
AD  - Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, People's Republic of China.
FAU - Wang, Wei
AU  - Wang W
AD  - Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, People's Republic of China.
FAU - Luo, Xiang
AU  - Luo X
AD  - Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong 
      University of Science and Technology, Wuhan, 430030, People's Republic of China. 
      tjhfile@tjh.tjmu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20160924
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (Cyclins)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Brain/cytology/*metabolism
MH  - Cell Hypoxia
MH  - Cells, Cultured
MH  - Cyclins/genetics/metabolism
MH  - *G2 Phase Cell Cycle Checkpoints
MH  - Glucose/*deficiency
MH  - *MAP Kinase Signaling System
MH  - Male
MH  - Oxygen/*metabolism
MH  - Pericytes/*metabolism/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
OTO - NOTNLM
OT  - Cell cycle
OT  - ERK
OT  - Oxygen-glucose deprivation
OT  - Pericyte
EDAT- 2016/09/26 06:00
MHDA- 2017/03/30 06:00
CRDT- 2016/09/26 06:00
PHST- 2016/06/20 00:00 [received]
PHST- 2016/09/13 00:00 [accepted]
PHST- 2016/09/26 06:00 [pubmed]
PHST- 2017/03/30 06:00 [medline]
PHST- 2016/09/26 06:00 [entrez]
AID - 10.1007/s12031-016-0844-2 [pii]
AID - 10.1007/s12031-016-0844-2 [doi]
PST - ppublish
SO  - J Mol Neurosci. 2017 Jan;61(1):105-114. doi: 10.1007/s12031-016-0844-2. Epub 2016 
      Sep 24.