PMID- 22709928
OWN - NLM
STAT- MEDLINE
DCOM- 20130610
LR  - 20211021
IS  - 1742-2094 (Electronic)
IS  - 1742-2094 (Linking)
VI  - 9
DP  - 2012 Jun 18
TI  - Increase of arginase activity in old apolipoprotein-E deficient mice under 
      Western diet associated with changes in neurovascular unit.
PG  - 132
LID - 10.1186/1742-2094-9-132 [doi]
AB  - Aging and atherosclerosis are well-recognized risk factors for cardiac and 
      neurovascular diseases. The Apolipoprotein E deficient (ApoE-/-) mouse on a 
      high-fat diet is a classical model of atherosclerosis, characterized by the 
      presence of atherosclerotic plaques in extracranial vessels but not in cerebral 
      arteries. Increase in arginase activity was shown to participate in vascular 
      dysfunction in the peripheral arteries of atherosclerotic mice by changing the 
      level of nitric oxide (NO). NO plays a key role in the physiological functions of 
      the neurovascular unit (NVU). However, the regulation of arginase expression and 
      activity in the brain was never investigated in association with changes in the 
      NVU, ApoE deficiency and high fat diet.Fourteen-month-old ApoE-/- mice on 
      high-fat diet exhibited deposition of lipids in the NVU, impairment of 
      blood-brain barrier properties, astrogliosis and an increase of aquaporin 4 
      staining. In association with these changes, brain arginase activity was 
      significantly increased in the old ApoE-/- mice as compared to old wild type 
      mice, with an increase in the level of arginase type I in the blood vessels.In 
      conclusion, aging in this classical mouse model of atherosclerosis induces an 
      increase in the level and activity of arginase I that may impair NO synthesis and 
      contribute to changes in the NVU leading to blood-brain barrier leakage and 
      inflammation.
FAU - Badaut, Jerome
AU  - Badaut J
AD  - Departments of Pediatrics and Physiology, Linda University School of Medicine, 
      Coleman Pavilion, Room A1120, 11175 Campus Street, Loma Linda, CA 92354, USA. 
      Jbadaut@llu.edu
FAU - Copin, Jean-Christophe
AU  - Copin JC
FAU - Fukuda, Andrew M
AU  - Fukuda AM
FAU - Gasche, Yvan
AU  - Gasche Y
FAU - Schaller, Karl
AU  - Schaller K
FAU - da Silva, Rafaela F
AU  - da Silva RF
LA  - eng
GR  - R01HD061946/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120618
PL  - England
TA  - J Neuroinflammation
JT  - Journal of neuroinflammation
JID - 101222974
RN  - 0 (Apolipoproteins E)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 3.5.3.1 (Arg1 protein, mouse)
RN  - EC 3.5.3.1 (Arginase)
SB  - IM
MH  - Aging/genetics/*metabolism/pathology
MH  - Animals
MH  - Apolipoproteins E/*deficiency/genetics
MH  - Arginase/genetics/*metabolism
MH  - Atherosclerosis/*enzymology/genetics/physiopathology
MH  - Blood-Brain Barrier/*enzymology/physiopathology
MH  - Diet, High-Fat/*adverse effects
MH  - Enzyme Activation/genetics
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Nitric Oxide/metabolism
MH  - Up-Regulation/*genetics
PMC - PMC3419627
EDAT- 2012/06/20 06:00
MHDA- 2013/06/12 06:00
PMCR- 2012/06/18
CRDT- 2012/06/20 06:00
PHST- 2011/12/22 00:00 [received]
PHST- 2012/06/18 00:00 [accepted]
PHST- 2012/06/20 06:00 [entrez]
PHST- 2012/06/20 06:00 [pubmed]
PHST- 2013/06/12 06:00 [medline]
PHST- 2012/06/18 00:00 [pmc-release]
AID - 1742-2094-9-132 [pii]
AID - 10.1186/1742-2094-9-132 [doi]
PST - epublish
SO  - J Neuroinflammation. 2012 Jun 18;9:132. doi: 10.1186/1742-2094-9-132.