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コーパス検索結果 (１語後でソート)

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1 ns are fatty streaks composed of lipid-laden macrophages (foam cells).
2 hich accumulated cholesterol is removed from macrophage foam cells.
3 receptor-mediated uptake, and transform into macrophage foam cells.
4 ression profile associated with inflammatory macrophage foam cells.
5 d ability to promote cholesterol efflux from macrophage foam cells.
6 r uptake is a newly characterized pathway in macrophage foam cells.
7  of inflammatory-response genes, observed in macrophage foam cells.
8  low-density lipoproteins (LDLs), generating macrophage foam cells.
9 disease by promoting cholesterol efflux from macrophage foam cells.
10 ained significantly higher numbers of viable macrophage foam cells.
11 filtration of the myocardium and spleen with macrophage foam cells.
12  increased phagocytosis and efferocytosis in macrophage foam cells.
13 sporter, ABCA1, that clears cholesterol from macrophage foam cells.
14 egrin adhesion receptors, is up-regulated on macrophage foam cells.
15  is a novel endocytic pathway that generates macrophage foam cells.
16 A-FN is localized with endothelial cells and macrophage foam cells.
17 e mechanism by which lipids are removed from macrophage foam cells.
18 emnants (extracellular lipid) in addition to macrophage foam cells.
19  contribute to the formation of both SMC and macrophage foam cells.
20  significantly increased in VSMC, but not in macrophage, foam cells.
21 not yet been determined whether lipid-loaded macrophages (foam cells), a major cellular component of
22                      Cholesterol efflux from macrophage foam cells, a key step in reverse cholesterol
23                                 Lipid-loaded macrophage "foam cells" accumulate in the subendothelial
24  beneficial but rather induced a significant macrophage foam cell accumulation in murine atherosclero
25  whereby HDL removes cholesterol from plaque macrophage foam cells and delivers it to the liver for p
26 arently mediate the cytotoxicity of oxLDL in macrophage foam cells and endothelial cells.
27 ux from VSMC foam cells was poor relative to macrophage foam cells, and largely occurs when HDL (high
28 ells immunoreacted for endothelial cell NOS; macrophages, foam cells, and smooth muscle cells immunos
29                           Cholesterol-loaded macrophage foam cells are a central component of atheros
30                            Cholesterol-laden macrophage foam cells are a hallmark of atherosclerosis.
31                             Inflammation and macrophage foam cells are characteristic features of ath
32                                              Macrophage foam cells are integral in the development of
33          We conclude that IL-8 is induced in macrophage foam cells as a response to cholesterol loadi
34 rther, MafB promotes cholesterol efflux from macrophage foam cells by directly up-regulating its key
35  Such damage may facilitate the formation of macrophage foam cells by impairing cholesterol efflux by
36  Accumulation of cholesteryl esters (CEs) in macrophage foam cells, central to atherosclerotic plaque
37 density lipoprotein (LDL) cholesterol-loaded macrophage foam cells contributes to the development of
38 domic and transcriptomic analysis of in vivo macrophage foam cells demonstrate that desmosterol is a
39 poprotein to promote cholesterol efflux from macrophage foam cells, direct experimental support for t
40 ulocyte colony stimulating factor in splenic macrophage foam cells, driving BM monocyte and neutrophi
41 -dependent binding, cholesterol loading, and macrophage foam cell formation after exposure to NO(2)-L
42 tein deposits and is known to be involved in macrophage foam cell formation and atherosclerosis.
43 B inhibited choline diet-enhanced endogenous macrophage foam cell formation and atherosclerotic lesio
44                                              Macrophage foam cell formation and cholesterol efflux, t
45  (LPS) has recently been shown to facilitate macrophage foam cell formation and has been suggested to
46 onstrate that an infectious agent can induce macrophage foam cell formation and implicate C. pneumoni
47 al anti-atherosclerotic effect by inhibiting macrophage foam cell formation and inflammation.
48 PS is a C. pneumoniae component that induces macrophage foam cell formation and suggest that infected
49    oxPC(CD36) accumulate in vivo and mediate macrophage foam cell formation as well as promote platel
50  anti-atherogenic cytokine TGF-beta inhibits macrophage foam cell formation by suppressing the expres
51                            This mechanism of macrophage foam cell formation does not depend on LDL mo
52 ll be useful in testing the role of ACAT and macrophage foam cell formation in atherosclerosis.
53 orption, hepatic lipoprotein production, and macrophage foam cell formation in atherosclerotic lesion
54 -CSF is a plausible mechanism to account for macrophage foam cell formation in atherosclerotic lesion
55 iponectin transgenic animals exhibit reduced macrophage foam cell formation in the arterial wall when
56  of GV sPLA2-modified LDL (GV-LDL) to induce macrophage foam cell formation in vitro.
57 ytoskeletal pathways that may be involved in macrophage foam cell formation in vivo but have been mis
58 -phase pinocytosis of LDL is a mechanism for macrophage foam cell formation in vivo.
59 ion of LDL that has the potential to promote macrophage foam cell formation independent of scavenger
60 y prevented: (i) oxLDL binding to CD36, (ii) macrophage foam cell formation induced by oxLDL, and (ii
61 sterase-treated LDL can cause human monocyte-macrophage foam cell formation inducing a 3-5-fold incre
62 molecular and cellular processes that govern macrophage foam cell formation is critical to understand
63                            In atherogenesis, macrophage foam cell formation is modulated by pathways
64 CD36 signaling, their role in CD36-dependent macrophage foam cell formation remains unknown.
65                                              Macrophage foam cell formation resulting from the accumu
66 acrophage cholesterol accumulation mimicking macrophage foam cell formation that occurs within athero
67 tivation of MC1-R confers protection against macrophage foam cell formation through a dual mechanism:
68 hlight an important role for KLF2 in primary macrophage foam cell formation via the potential regulat
69  effect of diet and LDL receptor genotype on macrophage foam cell formation within the peritoneal cav
70                 Chlamydia pneumoniae induces macrophage foam cell formation, a hallmark of early athe
71 as reported that C. pneumoniae induces human macrophage foam cell formation, a key event in early ath
72 ressed atherosclerosis, decreased peritoneal macrophage foam cell formation, and downregulated ER str
73 e in subendothelial lipoprotein aggregation, macrophage foam cell formation, and possibly other ather
74 n of APOC3-containing lipoprotein particles, macrophage foam cell formation, and the accelerated athe
75 of cytosolic lipid droplets is a hallmark of macrophage foam cell formation, and the molecular basics
76 ll proliferation, endothelial cell function, macrophage foam cell formation, as well as insulin secre
77  show that recombinant human PRG4 stimulates macrophage foam cell formation, but also dampens the pro
78 ers signaling cascades that are required for macrophage foam cell formation, but the mechanisms by wh
79 d compartments, and 2) causes human monocyte-macrophage foam cell formation.
80 n important component of ACAT regulation and macrophage foam cell formation.
81  for chlamydial lipopolysaccharide (cLPS) in macrophage foam cell formation.
82 tained on extracellular matrix and stimulate macrophage foam cell formation.
83 llular matrix and that are able to stimulate macrophage foam cell formation.
84 hesis that FFAR4 prevents the development of macrophage foam cell formation.
85 etinoid X receptor (RXR) activation and thus macrophage foam cell formation.
86 lerosis are independent of the regulation of macrophage foam cell formation.
87 herosclerosis, centered on the regulation of macrophage foam cell formation.
88 on of 25-hydroxycholesterol (25-HC) promotes macrophage foam cell formation.
89 ithm suggested that the TF ATF3 may regulate macrophage foam cell formation.
90 and Vavs in a signaling pathway required for macrophage foam cell formation.
91 ent in the development of atherosclerosis is macrophage foam cell formation.
92 sterol efflux and hence play a vital role in macrophage foam cell formation.
93 , impaired cholesterol efflux, and increased macrophage foam cell formation.
94 oteins in atherogenesis, with an emphasis on macrophage foam cell formation.
95 atherogenesis, including certain elements of macrophage foam cell formation.
96                 Anti-OxLDL CAR Tregs reduced macrophage foam-cell formation in vitro and significantl
97 ytokine-mediated immunosuppression to reduce macrophage foam-cell formation in vitro.
98 ing evidence implicating a role for ACAT1 in macrophage foam-cell formation, and for ACAT2 in intesti
99 ing cholesteryl esters as lipid droplets, in macrophage foam-cell formation, in absorbing dietary cho
100 ion, indicating that TZDs may not exacerbate macrophage foam-cell formation.
101 ed cells (CD68(+), primarily macrophages and macrophage foam cells) from plaques.
102 e recent data on the effects of estrogens on macrophage foam cell function.
103                                              Macrophage foam cells in atherosclerotic lesions accumul
104                          The accumulation of macrophage foam cells in atherosclerotic lesions is asso
105 d secretion of SMPDL3A by cholesterol-loaded macrophage foam cells in lesions may decrease local conc
106 rich lipoprotein degradation and uptake into macrophage foam cells in the arterial intima.
107 e A1, which promotes cholesterol efflux from macrophage foam cells in the arterial wall.
108 r disease by accepting free cholesterol from macrophage foam cells in the artery wall.
109 PPARbeta agonist, inhibited the formation of macrophage foam cells in the peritoneal cavity.
110 interaction of Lp(a) with cholesterol-loaded macrophages (foam cells) in atheromata may be important
111 opy and immunohistochemistry showed abundant macrophage foam cells, indicating that lipid uptake by i
112          Injection of 3H-cholesterol-labeled macrophage foam cells is a method of measuring reverse c
113         Gene expression analysis of lesional macrophage foam cells is complicated by the cellular het
114  shows that cholesterol efflux capacity from macrophage foam cells is not associated with cardiovascu
115 blished over the past few years suggest that macrophage foam cells may also be an important site of e
116             PPARgamma is highly expressed in macrophage foam cells of atherosclerotic lesions and has
117 e demonstrate that PPARgamma is expressed in macrophage foam cells of human atherosclerotic lesions,
118         These data demonstrate that VSMC and macrophage foam cells perform cholesterol efflux by dist
119         We further demonstrate activation of macrophage/foam cell PI3-kinase/Akt in atherosclerotic p
120             We showed that in vivo generated macrophage foam cells produce superoxide, nitric oxide,
121                 In advanced atherosclerosis, macrophage foam cells progressively accumulate large amo
122 f modified LDL in the presence of C1q alters macrophage foam cell survival or function.
123 nd probably mediates cholesterol efflux from macrophage foam cells to the major HDL fractions, provid
124 proteins can promote cholesterol efflux from macrophage foam cells via the ATP-binding cassette trans
125              C pneumoniae, frequently within macrophage foam cells, was identified in coronary fibrol
126                                              Macrophage foam cells were depleted in mPGES-1(-/-) LDLR
127 as elucidated a mechanism for development of macrophage foam cells when macrophages are incubated wit
128 osclerotic lesion is mediated by lipid-laden macrophages (foam cells), which also establish chronic i
129  capacity was quantified by incubating human macrophage foam cells with apoB-depleted serum.
130 CEC was quantified using incubation of human macrophage foam cells with apolipoprotein B-depleted pla
131 ine was quantified using incubation of human macrophage foam cells with apolipoprotein B-depleted pla
132 ecrotic granulomas contain triglyceride-rich macrophages (foam cells) with reduced antimicrobial func
133 poprotein, a key event in the development of macrophage foam cells within atherosclerotic lesions.
134                                 Furthermore, macrophage foam cells within lesions of the IL-10 Tg gro
135 facilitates cellular cholesterol efflux from macrophage foam cells within the intima of the lesion.

 
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