PMID- 21919908
OWN - NLM
STAT- MEDLINE
DCOM- 20111223
LR  - 20211020
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 119
IP  - 4
DP  - 2011 Nov
TI  - Oxygen-glucose deprivation and interleukin-1alpha trigger the release of perlecan LG3 
      by cells of neurovascular unit.
PG  - 760-71
LID - 10.1111/j.1471-4159.2011.07484.x [doi]
AB  - Two of the main stresses faced by cells at the neurovascular unit (NVU) as an 
      immediate result of cerebral ischemia are oxygen-glucose deprivation 
      (OGD)/reperfusion and inflammatory stress caused by up regulation of IL-1. As a 
      result of these stresses, perlecan, an important component of the NVU 
      extracellular matrix, is highly proteolyzed. In this study, we describe that 
      focal cerebral ischemia in rats results in increased generation of laminin 
      globular domain 3 (LG3), the c-terminal bioactive fragment of perlecan. Further, 
      in vitro study of the cells of the NVU was performed to locate the source of this 
      increased perlecan-LG3. Neurons, astrocytes, brain endothelial cells and 
      pericytes were exposed to OGD/reperfusion and IL-1alpha/beta. It was observed that 
      neurons and pericytes showed increased levels of LG3 during OGD in their culture 
      media. During in vitro reperfusion, neurons, astrocytes and pericytes showed 
      elevated levels of LG3, but only after exposure to brief durations of OGD. IL-1alpha 
      and IL-1beta treatment tended to have opposite effects on NVU cells. While IL-1alpha 
      increased or had minimal to no effect on LG3 generation, high concentrations of 
      IL-1beta decreased it in most cells studied. Finally, LG3 was determined to be 
      neuroprotective and anti-proliferative in brain endothelial cells, suggesting a 
      possible role for the generation of LG3 in the ischemic brain.
CI  - (c) 2011 The Authors. Journal of Neurochemistry (c) 2011 International Society for 
      Neurochemistry.
FAU - Saini, Maxim G
AU  - Saini MG
AD  - Department of Molecular and Cellular Medicine, Texas A&M College of Medicine, 
      College Station, Texas 77843, USA.
FAU - Pinteaux, Emmanuel
AU  - Pinteaux E
FAU - Lee, Boyeon
AU  - Lee B
FAU - Bix, Gregory J
AU  - Bix GJ
LA  - eng
GR  - R01 NS065842/NS/NINDS NIH HHS/United States
GR  - R01 NS065842-01A1/NS/NINDS NIH HHS/United States
GR  - R01NS065842-01A01/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20111011
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Heparan Sulfate Proteoglycans)
RN  - 0 (Interleukin-1alpha)
RN  - 0 (Interleukin-1beta)
RN  - 143972-95-6 (perlecan)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Animals, Newborn
MH  - Astrocytes/drug effects/metabolism
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Embryo, Mammalian
MH  - Endothelial Cells/drug effects/metabolism
MH  - Glucose/*deficiency
MH  - Heparan Sulfate Proteoglycans/genetics/*metabolism
MH  - Humans
MH  - Hypoxia/*metabolism
MH  - Infarction, Middle Cerebral Artery/*metabolism/pathology
MH  - Interleukin-1alpha/*pharmacology
MH  - Interleukin-1beta/pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neurons/drug effects/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Up-Regulation/*drug effects/physiology
PMC - PMC3197937
MID - NIHMS325790
EDAT- 2011/09/17 06:00
MHDA- 2011/12/24 06:00
PMCR- 2012/11/01
CRDT- 2011/09/17 06:00
PHST- 2011/09/17 06:00 [entrez]
PHST- 2011/09/17 06:00 [pubmed]
PHST- 2011/12/24 06:00 [medline]
PHST- 2012/11/01 00:00 [pmc-release]
AID - 10.1111/j.1471-4159.2011.07484.x [doi]
PST - ppublish
SO  - J Neurochem. 2011 Nov;119(4):760-71. doi: 10.1111/j.1471-4159.2011.07484.x. Epub 
      2011 Oct 11.