Pubmed-entry ::= {
pmid 22556334,
medent {
em std {
year 2012,
month 5,
day 17
},
cit {
title {
name "Macrophage-derived angiopoietin-like protein 2 accelerates
development of abdominal aortic aneurysm."
},
authors {
names ml {
"Tazume H",
"Miyata K",
"Tian Z",
"Endo M",
"Horiguchi H",
"Takahashi O",
"Horio E",
"Tsukano H",
"Kadomatsu T",
"Nakashima Y",
"Kunitomo R",
"Kaneko Y",
"Moriyama S",
"Sakaguchi H",
"Okamoto K",
"Hara M",
"Yoshinaga T",
"Yoshimura K",
"Aoki H",
"Araki K",
"Hao H",
"Kawasuji M",
"Oike Y"
},
affil str "Department of Molecular Genetics, Graduate School of
Medical Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto
860-8556, Japan. oike@gpo.kumamoto-u.ac.jp."
},
from journal {
title {
iso-jta "Arterioscler. Thromb. Vasc. Biol.",
ml-jta "Arterioscler Thromb Vasc Biol",
issn "1524-4636",
name "Arteriosclerosis, thrombosis, and vascular biology"
},
imp {
date std {
year 2012,
month 6
},
volume "32",
issue "6",
pages "1400-1409",
language "eng",
pubstatus ppublish,
history {
{
pubstatus aheadofprint,
date std {
year 2012,
month 5,
day 3
}
},
{
pubstatus other,
date std {
year 2012,
month 5,
day 5,
hour 6,
minute 0
}
},
{
pubstatus pubmed,
date std {
year 2012,
month 5,
day 5,
hour 6,
minute 0
}
},
{
pubstatus medline,
date std {
year 2012,
month 5,
day 5,
hour 6,
minute 0
}
}
}
}
},
ids {
pii "ATVBAHA.112.247866",
doi "10.1161/ATVBAHA.112.247866",
pubmed 22556334
}
},
abstract "OBJECTIVE: Recently, we reported that angiopoietin-like protein
2 (Angptl2) functions in various chronic inflammatory diseases. In the
present study, we asked whether Angptl2 and its associated chronic
inflammation contribute to abdominal aortic aneurysm (AAA). METHODS AND
RESULTS: Immunohistochemistry revealed that Angptl2 is abundantly expressed
in infiltrating macrophages within the vessel wall of patients with AAA and
in a CaCl(2)-induced AAA mouse model. When Angptl2-deficient mice were used
in the mouse model, they showed decreased AAA development compared with
wild-type mice, as evidenced by reduction in aneurysmal size, less severe
destruction of vessel structure, and lower expression of proinflammatory
cytokines and matrix metalloproteinase-9. However, no difference in the
number of infiltrating macrophages within the aortic aneurysmal vessel wall
was observed between genotypes. AAA development was also significantly
suppressed in wild-type mice that underwent Angptl2-deficient bone marrow
transplantation. Expression levels of proinflammatory cytokines and
metalloproteinase-9 in Angptl2-deficient macrophages were significantly
decreased, and those decreases were rescued by treatment of Angptl2 deficient
macrophages with exogenous Angptl2. CONCLUSIONS: Macrophage-derived Angptl2
contributes to AAA development by inducing inflammation and degradation of
extracellular matrix in the vessel wall, suggesting that targeting the
Angptl2-induced inflammatory axis in macrophages could represent a new
strategy for AAA therapy.",
pmid 22556334,
pub-type {
"Journal Article"
},
status premedline
}
}
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