PMID- 25600958
OWN - NLM
STAT- MEDLINE
DCOM- 20151201
LR  - 20150227
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 289
DP  - 2015 Mar 19
TI  - Damage effect of interleukin (IL)-23 on oxygen-glucose-deprived cells of the 
      neurovascular unit via IL-23 receptor.
PG  - 406-16
LID - S0306-4522(15)00060-3 [pii]
LID - 10.1016/j.neuroscience.2015.01.012 [doi]
AB  - Interleukin-23/interleukin-23 receptor (IL-23/IL-23R) has been implicated in many 
      inflammatory diseases. Previous research mainly focused on its ability to induce 
      IL-17 production from T cells. However, few studies have investigated its role in 
      cerebral ischemic injury. The aim of our study was to explore the potential 
      effect of IL-23 on cells of the neurovascular unit (NVU) under an oxygen-glucose 
      deprivation (OGD) condition and the role of IL-23R in IL-23-mediated effect. OGD 
      of primary cells of the NVU and permanent middle cerebral artery occlusion 
      (pMCAO) were used to produce experimental stroke in vitro and in vivo, 
      respectively. IL-23 and IL-23R were detected by immunohistochemistry and western 
      blot in pMCAO mice. Metabolic viability of cultured cells was assessed by MTT 
      assay. The cell-associated proteins (Bcl-2, AQP4 and ET-1) were determined by 
      western blot and enzyme-linked immunosorbent assay (ELISA). Immunofluorescence 
      staining and western blot were used to detect the IL-23R expression. The results 
      showed that the expression of IL-23/IL-23R was elevated in pMCAO mice. IL-23 
      could aggravate neuron damage, astrocyte swelling, and further impair the 
      integrity of blood-brain barrier induced by OGD. In addition, the effect of IL-23 
      on cells of the NVU is mediated by IL-23R and is likely IL-23R-expression-level 
      dependent. However, there are no such biological properties for the IL-23p19 
      subunit alone. Our study provides the first evidence that IL-23 has a toxic 
      effect on cells of the NVU under OGD stress, which is mediated by IL-23R. These 
      results not only help us better understand the role of IL-23/IL-23R in brain 
      ischemia, but also provide a potential therapeutic target in stroke.
CI  - Copyright (c) 2015 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Wang, M
AU  - Wang M
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China.
FAU - Zhong, D
AU  - Zhong D
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China.
FAU - Zheng, Y
AU  - Zheng Y
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China.
FAU - Li, H
AU  - Li H
AD  - Department of Neurobiology, Harbin Medical University Provincial Key Lab of 
      Neurobiology, Harbin Medical University, Xuefu Road, 150081 Heilongjiang, PR 
      China.
FAU - Chen, H
AU  - Chen H
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China.
FAU - Ma, S
AU  - Ma S
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China.
FAU - Sun, Y
AU  - Sun Y
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China.
FAU - Yan, W
AU  - Yan W
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China.
FAU - Li, G
AU  - Li G
AD  - Department of Neurology, The First Affiliated Hospital, Harbin Medical 
      University, 23 You Zheng Street, Harbin, 150001 Heilongjiang, PR China. 
      Electronic address: hydlgz1962@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150116
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Interleukin-23)
RN  - 0 (Receptors, Interleukin)
RN  - 0 (interleukin-23 receptor, mouse)
RN  - 0 (interleukin-23 receptor, rat)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism/pathology
MH  - Blood-Brain Barrier/metabolism/pathology
MH  - Brain/metabolism/pathology
MH  - Brain Ischemia/metabolism/pathology
MH  - Capillary Permeability/physiology
MH  - Cell Hypoxia/*physiology
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Endothelial Cells/metabolism/pathology
MH  - Glucose/*deficiency
MH  - Infarction, Middle Cerebral Artery
MH  - Interleukin-23/*metabolism
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Neurons/metabolism/pathology
MH  - Rats, Wistar
MH  - Receptors, Interleukin/*metabolism
MH  - Stroke/*metabolism/pathology
OTO - NOTNLM
OT  - IL-23
OT  - IL-23R
OT  - cerebral ischemic injury
OT  - p19 subunit
EDAT- 2015/01/21 06:00
MHDA- 2015/12/15 06:00
CRDT- 2015/01/21 06:00
PHST- 2014/07/22 00:00 [received]
PHST- 2015/01/08 00:00 [revised]
PHST- 2015/01/08 00:00 [accepted]
PHST- 2015/01/21 06:00 [entrez]
PHST- 2015/01/21 06:00 [pubmed]
PHST- 2015/12/15 06:00 [medline]
AID - S0306-4522(15)00060-3 [pii]
AID - 10.1016/j.neuroscience.2015.01.012 [doi]
PST - ppublish
SO  - Neuroscience. 2015 Mar 19;289:406-16. doi: 10.1016/j.neuroscience.2015.01.012. 
      Epub 2015 Jan 16.