PMID- 20877383
OWN - NLM
STAT- MEDLINE
DCOM- 20110427
LR  - 20211020
IS  - 1559-7016 (Electronic)
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 31
IP  - 3
DP  - 2011 Mar
TI  - Vascular adhesion protein-1 inhibition provides antiinflammatory protection after 
      an intracerebral hemorrhagic stroke in mice.
PG  - 881-93
LID - 10.1038/jcbfm.2010.167 [doi]
AB  - The systemic immune response has a vital role in propagating the damage of an 
      intracerebral hemorrhage (ICH). Vascular adhesion protein-1 (VAP-1), a 
      semicarbazide (SCZ)-sensitive-amine-oxidase, was found in previous studies to 
      have a role in migration of immune cells. In this study, we hypothesize that 
      VAP-1 inhibition may decrease brain injury by attenuating the transmigration of 
      immune cells to the injury site, and by doing so, reduce cerebral edema and 
      improve neurobehavioral function in mice. Two VAP-1 inhibitors, LJP1586 and SCZ 
      were given 1 hour after ICH induction by either collagenase or autologous blood 
      injection. The VAP-1 siRNA, a VAP-1 gene silencer, and human recombinant AOC3 
      protein, a VAP-1 analogue, were delivered by intracerebroventricular injection. 
      Postassessment included neurobehavioral testing, brain edema measurement, 
      quantification of neutrophil infiltration and microglia/macrophage activation, 
      and measurement of intercellular adhesion molecule-1 (ICAM-1), P-selectin, 
      monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-alpha) 
      expression 24 hours after ICH. We found that LJP1586 and SCZ reduced brain edema 
      and neurobehavioral deficits 24 hours after ICH induction. These two drugs were 
      also found to decrease levels of ICAM-1, MCP-1, TNF-alpha, and inhibit neutrophilic 
      infiltration and microglia/macrophage activation. We conclude that VAP-1 
      inhibition provided antiinflammation effect by reducing adhesion molecule 
      expression and immune cell infiltration after ICH.
FAU - Ma, Qingyi
AU  - Ma Q
AD  - Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, 
      California 92354, USA.
FAU - Manaenko, Anatol
AU  - Manaenko A
FAU - Khatibi, Nikan H
AU  - Khatibi NH
FAU - Chen, Wanqiu
AU  - Chen W
FAU - Zhang, John H
AU  - Zhang JH
FAU - Tang, Jiping
AU  - Tang J
LA  - eng
GR  - R01 NS053407/NS/NINDS NIH HHS/United States
GR  - R01 NS060936/NS/NINDS NIH HHS/United States
GR  - NS060936/NS/NINDS NIH HHS/United States
GR  - NS053407/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20100929
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the 
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (3-fluoro-2-(4-methoxybenzyl)allylamine)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Semicarbazides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 37QUC23K2X (carbamylhydrazine)
RN  - 48G762T011 (Allylamine)
RN  - EC 1.4.3.21 (AOC3 protein, human)
RN  - EC 1.4.3.21 (Amine Oxidase (Copper-Containing))
RN  - EC 1.4.3.21 (semicarbazide-sensitive amine oxidase-vascular adhesion protein-1, 
      mouse)
SB  - IM
MH  - Allylamine/administration & dosage/*analogs & derivatives/antagonists & 
      inhibitors
MH  - Amine Oxidase (Copper-Containing)/administration & dosage/*antagonists & 
      inhibitors/genetics
MH  - Animals
MH  - Behavior, Animal/drug effects
MH  - Brain Edema/pathology
MH  - Cell Adhesion Molecules/administration & dosage/*antagonists & 
      inhibitors/genetics
MH  - Chemokine CCL2/metabolism
MH  - Down-Regulation
MH  - Gene Silencing
MH  - Humans
MH  - Inflammation/*etiology/*prevention & control
MH  - Injections, Intraperitoneal
MH  - Injections, Intraventricular
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Intracranial Hemorrhages/*complications/pathology/physiopathology/psychology
MH  - Male
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Nervous System/drug effects/physiopathology
MH  - Neutrophil Infiltration/drug effects
MH  - RNA, Small Interfering/administration & dosage
MH  - Recombinant Proteins/administration & dosage
MH  - Semicarbazides/administration & dosage
MH  - Stroke/*complications/etiology
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC3063621
EDAT- 2010/09/30 06:00
MHDA- 2011/04/28 06:00
PMCR- 2012/03/01
CRDT- 2010/09/30 06:00
PHST- 2010/09/30 06:00 [entrez]
PHST- 2010/09/30 06:00 [pubmed]
PHST- 2011/04/28 06:00 [medline]
PHST- 2012/03/01 00:00 [pmc-release]
AID - jcbfm2010167 [pii]
AID - 10.1038/jcbfm.2010.167 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2011 Mar;31(3):881-93. doi: 10.1038/jcbfm.2010.167. 
      Epub 2010 Sep 29.