PMID- 27717824
OWN - NLM
STAT- MEDLINE
DCOM- 20170606
LR  - 20170606
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 480
IP  - 1
DP  - 2016 Nov 4
TI  - MyD88 contributes to neuroinflammatory responses induced by cerebral 
      ischemia/reperfusion in mice.
PG  - 69-74
LID - S0006-291X(16)31662-X [pii]
LID - 10.1016/j.bbrc.2016.10.007 [doi]
AB  - Myeloid differentiation primary-response protein-88 (MyD88) is one of adaptor 
      proteins mediating Toll-like receptors (TLRs) signaling. Activation of MyD88 
      results in the activation of nuclear factor kappa B (NFkappaB) and the increase of 
      inflammatory responses. Evidences have demonstrated that TLRs signaling 
      contributes to cerebral ischemia/reperfusion (I/R) injury. However, the role of 
      MyD88 in this mechanism of action is disputed and needs to be clarified. In the 
      present study, in a mouse model of cerebral I/R, we examined the activities of 
      NFkappaB and interferon factor-3 (IRF3), and the inflammatory responses in ischemic 
      brain tissue using ELISA, Western blots, and real-time PCR. Neurological function 
      and cerebral infarct size were also evaluated 24 h after cerebral I/R. Our 
      results showed that NFkappaB activity increased in ischemic brains, but IRF3 was not 
      activated after cerebral I/R, in wild-type (WT) mice. MyD88 deficit inhibited the 
      activation of NFkappaB, and the expression of interleukin-1beta (IL-1beta), IL-6, Beclin-1 
      (BECN1), pellino-1, and cyclooxygenase-2 (COX-2) increased by cerebral I/R 
      compared with WT mice. Interestingly, the expression of interferon Beta 1 (INFB1) 
      and vascular endothelial growth factor (VEGF) increased in MyD88 KO mice. 
      Unexpectedly, although the neurological function improved in the MyD88 knockout 
      (KO) mice, the deficit of MyD88 failed to reduce cerebral infarct size compared 
      to WT mice. We concluded that MyD88-dependent signaling contributes to the 
      inflammatory responses induced by cerebral I/R. MyD88 deficit may inhibit the 
      increased inflammatory response and increase neuroprotective signaling.
CI  - Copyright (c) 2016 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Ye, Xinchun
AU  - Ye X
AD  - Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, 
      Xuzhou 221002, China.
FAU - Kong, Delian
AU  - Kong D
AD  - Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, 
      Xuzhou 221002, China.
FAU - Wang, Jun
AU  - Wang J
AD  - Department of Emergency Medicine, Emory University School of Medicine, Atlanta, 
      GA, USA.
FAU - Ishrat, Tauheed
AU  - Ishrat T
AD  - Department of Emergency Medicine, Emory University School of Medicine, Atlanta, 
      GA, USA.
FAU - Shi, Hongjuan
AU  - Shi H
AD  - Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, 
      Xuzhou 221002, China.
FAU - Ding, Xiaohui
AU  - Ding X
AD  - Department of Human Anatomy, Histology and Embryology, Shenyang Medical College, 
      Shenyang, 110000, China.
FAU - Cui, Guiyun
AU  - Cui G
AD  - Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, 
      Xuzhou 221002, China.
FAU - Hua, Fang
AU  - Hua F
AD  - Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, 
      Xuzhou 221002, China; Department of Emergency Medicine, Emory University School 
      of Medicine, Atlanta, GA, USA; Key Laboratory of Anesthesiology of Jiangsu 
      Province, Xuzhou 221002, China. Electronic address: huafang@xzhmu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20161004
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Beclin-1)
RN  - 0 (Becn1 protein, mouse)
RN  - 0 (Interferon Regulatory Factor-3)
RN  - 0 (Irf3 protein, mouse)
RN  - 0 (Myd88 protein, mouse)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (NF-kappa B)
RN  - EC 1.14.99.- (Ptgs2 protein, mouse)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
SB  - IM
MH  - Animals
MH  - Beclin-1/metabolism
MH  - Blotting, Western
MH  - Brain Infarction/metabolism/pathology
MH  - Brain Ischemia/metabolism/*physiopathology
MH  - Cyclooxygenase 2/metabolism
MH  - Encephalitis/*metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Interferon Regulatory Factor-3/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Myeloid Differentiation Factor 88/genetics/*metabolism
MH  - NF-kappa B/metabolism
MH  - Real-Time Polymerase Chain Reaction
MH  - Reperfusion Injury/metabolism/*physiopathology
OTO - NOTNLM
OT  - Cerebral ischemia/reperfusion injury
OT  - Inflammatory responses
OT  - MyD88-dependent pathway
OT  - Toll-like receptors
EDAT- 2016/10/21 06:00
MHDA- 2017/06/07 06:00
CRDT- 2016/10/09 06:00
PHST- 2016/09/22 00:00 [received]
PHST- 2016/10/03 00:00 [accepted]
PHST- 2016/10/21 06:00 [pubmed]
PHST- 2017/06/07 06:00 [medline]
PHST- 2016/10/09 06:00 [entrez]
AID - S0006-291X(16)31662-X [pii]
AID - 10.1016/j.bbrc.2016.10.007 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2016 Nov 4;480(1):69-74. doi: 
      10.1016/j.bbrc.2016.10.007. Epub 2016 Oct 4.