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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Neuropathol+Exp+Neurol
2016 ; 75
(7
): 689-99
Nephropedia Template TP
gab.com Text
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English Wikipedia
Smooth Muscle Cell Foam Cell Formation, Apolipoproteins, and ABCA1 in
Intracranial Aneurysms: Implications for Lipid Accumulation as a Promoter of
Aneurysm Wall Rupture
#MMPMID27283327
Ollikainen E
; Tulamo R
; Lehti S
; Lee-Rueckert M
; Hernesniemi J
; Niemelä M
; Ylä-Herttuala S
; Kovanen PT
; Frösen J
J Neuropathol Exp Neurol
2016[Jul]; 75
(7
): 689-99
PMID27283327
show ga
Saccular intracranial aneurysm (sIA) aneurysm causes intracranial hemorrhages
that are associated with high mortality. Lipid accumulation and chronic
inflammation occur in the sIA wall. A major mechanism for lipid clearance from
arteries is adenosine triphosphate-binding cassette A1 (ABCA1)-mediated lipid
efflux from foam cells to apolipoprotein A-I (apoA-I). We investigated the
association of wall degeneration, inflammation, and lipid-related parameters in
tissue samples of 16 unruptured and 20 ruptured sIAs using histology and
immunohistochemistry. Intracellular lipid accumulation was associated with wall
remodeling (p?=?0.005) and rupture (p?=?0.020). Foam cell formation was observed
in smooth muscle cells, in addition to CD68- and CD163-positive macrophages.
Macrophage infiltration correlated with intracellular lipid accumulation and
apolipoproteins, including apoA-I. ApoA-I correlated with markers of lipid
accumulation and wall degeneration (p?=?0.01). ApoA-I-positive staining
colocalized with ABCA1-positive cells particularly in sIAs with high number of
smooth muscle cells (p?=?0.003); absence of such colocalization was associated
with wall degeneration (p?=?0.017). Known clinical risk factors for sIA rupture
correlated inversely with apoA-I. We conclude that lipid accumulation associates
with sIA wall degeneration and risk of rupture, possibly via formation of foam
cells and subsequent loss of mural cells. Reduced removal of lipids from the sIA
wall via ABCA1-apoA-I pathway may contribute to this process.