ライフサイエンスコーパス: macrophage foam cell

1 ns are fatty streaks composed of lipid-laden macrophages (foam cells).

2 low-density lipoproteins (LDLs), generating macrophage foam cells.

3 receptor-mediated uptake, and transform into macrophage foam cells.

4 d ability to promote cholesterol efflux from macrophage foam cells.

5 r uptake is a newly characterized pathway in macrophage foam cells.

6 of inflammatory-response genes, observed in macrophage foam cells.

7 increased phagocytosis and efferocytosis in macrophage foam cells.

8 disease by promoting cholesterol efflux from macrophage foam cells.

9 ained significantly higher numbers of viable macrophage foam cells.

10 filtration of the myocardium and spleen with macrophage foam cells.

11 sporter, ABCA1, that clears cholesterol from macrophage foam cells.

12 egrin adhesion receptors, is up-regulated on macrophage foam cells.

13 is a novel endocytic pathway that generates macrophage foam cells.

14 A-FN is localized with endothelial cells and macrophage foam cells.

15 e mechanism by which lipids are removed from macrophage foam cells.

16 emnants (extracellular lipid) in addition to macrophage foam cells.

17 contribute to the formation of both SMC and macrophage foam cells.

18 hich accumulated cholesterol is removed from macrophage foam cells.

19 not yet been determined whether lipid-loaded macrophages (foam cells), a major cellular component of

20 Cholesterol efflux from macrophage foam cells, a key step in reverse cholesterol

21 Lipid-loaded macrophage "foam cells" accumulate in the subendothelial

22 beneficial but rather induced a significant macrophage foam cell accumulation in murine atherosclero

23 arently mediate the cytotoxicity of oxLDL in macrophage foam cells and endothelial cells.

24 ells immunoreacted for endothelial cell NOS; macrophages, foam cells, and smooth muscle cells immunos

25 Cholesterol-loaded macrophage foam cells are a central component of atheros

26 Inflammation and macrophage foam cells are characteristic features of ath

27 Macrophage foam cells are integral in the development of

28 We conclude that IL-8 is induced in macrophage foam cells as a response to cholesterol loadi

29 rther, MafB promotes cholesterol efflux from macrophage foam cells by directly up-regulating its key

30 Such damage may facilitate the formation of macrophage foam cells by impairing cholesterol efflux by

31 Accumulation of cholesteryl esters (CEs) in macrophage foam cells, central to atherosclerotic plaque

32 density lipoprotein (LDL) cholesterol-loaded macrophage foam cells contributes to the development of

33 poprotein to promote cholesterol efflux from macrophage foam cells, direct experimental support for t

34 ulocyte colony stimulating factor in splenic macrophage foam cells, driving BM monocyte and neutrophi

35 -dependent binding, cholesterol loading, and macrophage foam cell formation after exposure to NO(2)-L

36 tein deposits and is known to be involved in macrophage foam cell formation and atherosclerosis.

37 B inhibited choline diet-enhanced endogenous macrophage foam cell formation and atherosclerotic lesio

38 Macrophage foam cell formation and cholesterol efflux, t

39 (LPS) has recently been shown to facilitate macrophage foam cell formation and has been suggested to

40 onstrate that an infectious agent can induce macrophage foam cell formation and implicate C. pneumoni

41 PS is a C. pneumoniae component that induces macrophage foam cell formation and suggest that infected

42 oxPC(CD36) accumulate in vivo and mediate macrophage foam cell formation as well as promote platel

43 anti-atherogenic cytokine TGF-beta inhibits macrophage foam cell formation by suppressing the expres

44 This mechanism of macrophage foam cell formation does not depend on LDL mo

45 ll be useful in testing the role of ACAT and macrophage foam cell formation in atherosclerosis.

46 orption, hepatic lipoprotein production, and macrophage foam cell formation in atherosclerotic lesion

47 -CSF is a plausible mechanism to account for macrophage foam cell formation in atherosclerotic lesion

48 iponectin transgenic animals exhibit reduced macrophage foam cell formation in the arterial wall when

49 of GV sPLA2-modified LDL (GV-LDL) to induce macrophage foam cell formation in vitro.

50 ytoskeletal pathways that may be involved in macrophage foam cell formation in vivo but have been mis

51 -phase pinocytosis of LDL is a mechanism for macrophage foam cell formation in vivo.

52 ion of LDL that has the potential to promote macrophage foam cell formation independent of scavenger

53 y prevented: (i) oxLDL binding to CD36, (ii) macrophage foam cell formation induced by oxLDL, and (ii

54 sterase-treated LDL can cause human monocyte-macrophage foam cell formation inducing a 3-5-fold incre

55 molecular and cellular processes that govern macrophage foam cell formation is critical to understand

56 In atherogenesis, macrophage foam cell formation is modulated by pathways

57 CD36 signaling, their role in CD36-dependent macrophage foam cell formation remains unknown.

58 Macrophage foam cell formation resulting from the accumu

59 acrophage cholesterol accumulation mimicking macrophage foam cell formation that occurs within athero

60 tivation of MC1-R confers protection against macrophage foam cell formation through a dual mechanism:

61 hlight an important role for KLF2 in primary macrophage foam cell formation via the potential regulat

62 effect of diet and LDL receptor genotype on macrophage foam cell formation within the peritoneal cav

63 Chlamydia pneumoniae induces macrophage foam cell formation, a hallmark of early athe

64 as reported that C. pneumoniae induces human macrophage foam cell formation, a key event in early ath

65 ressed atherosclerosis, decreased peritoneal macrophage foam cell formation, and downregulated ER str

66 e in subendothelial lipoprotein aggregation, macrophage foam cell formation, and possibly other ather

67 of cytosolic lipid droplets is a hallmark of macrophage foam cell formation, and the molecular basics

68 ll proliferation, endothelial cell function, macrophage foam cell formation, as well as insulin secre

69 ers signaling cascades that are required for macrophage foam cell formation, but the mechanisms by wh

70 n important component of ACAT regulation and macrophage foam cell formation.

71 for chlamydial lipopolysaccharide (cLPS) in macrophage foam cell formation.

72 tained on extracellular matrix and stimulate macrophage foam cell formation.

73 llular matrix and that are able to stimulate macrophage foam cell formation.

74 herosclerosis, centered on the regulation of macrophage foam cell formation.

75 on of 25-hydroxycholesterol (25-HC) promotes macrophage foam cell formation.

76 ithm suggested that the TF ATF3 may regulate macrophage foam cell formation.

77 and Vavs in a signaling pathway required for macrophage foam cell formation.

78 ent in the development of atherosclerosis is macrophage foam cell formation.

79 sterol efflux and hence play a vital role in macrophage foam cell formation.

80 , impaired cholesterol efflux, and increased macrophage foam cell formation.

81 oteins in atherogenesis, with an emphasis on macrophage foam cell formation.

82 atherogenesis, including certain elements of macrophage foam cell formation.

83 d compartments, and 2) causes human monocyte-macrophage foam cell formation.

84 ing evidence implicating a role for ACAT1 in macrophage foam-cell formation, and for ACAT2 in intesti

85 ing cholesteryl esters as lipid droplets, in macrophage foam-cell formation, in absorbing dietary cho

86 ion, indicating that TZDs may not exacerbate macrophage foam-cell formation.

87 ed cells (CD68(+), primarily macrophages and macrophage foam cells) from plaques.

88 e recent data on the effects of estrogens on macrophage foam cell function.

89 Macrophage foam cells in atherosclerotic lesions accumul

90 The accumulation of macrophage foam cells in atherosclerotic lesions is asso

91 d secretion of SMPDL3A by cholesterol-loaded macrophage foam cells in lesions may decrease local conc

92 rich lipoprotein degradation and uptake into macrophage foam cells in the arterial intima.

93 e A1, which promotes cholesterol efflux from macrophage foam cells in the arterial wall.

94 r disease by accepting free cholesterol from macrophage foam cells in the artery wall.

95 PPARbeta agonist, inhibited the formation of macrophage foam cells in the peritoneal cavity.

96 interaction of Lp(a) with cholesterol-loaded macrophages (foam cells) in atheromata may be important

97 opy and immunohistochemistry showed abundant macrophage foam cells, indicating that lipid uptake by i

98 Injection of 3H-cholesterol-labeled macrophage foam cells is a method of measuring reverse c

99 Gene expression analysis of lesional macrophage foam cells is complicated by the cellular het

100 shows that cholesterol efflux capacity from macrophage foam cells is not associated with cardiovascu

101 blished over the past few years suggest that macrophage foam cells may also be an important site of e

102 PPARgamma is highly expressed in macrophage foam cells of atherosclerotic lesions and has

103 e demonstrate that PPARgamma is expressed in macrophage foam cells of human atherosclerotic lesions,

104 We further demonstrate activation of macrophage/foam cell PI3-kinase/Akt in atherosclerotic p

105 We showed that in vivo generated macrophage foam cells produce superoxide, nitric oxide,

106 In advanced atherosclerosis, macrophage foam cells progressively accumulate large amo

107 f modified LDL in the presence of C1q alters macrophage foam cell survival or function.

108 nd probably mediates cholesterol efflux from macrophage foam cells to the major HDL fractions, provid

109 proteins can promote cholesterol efflux from macrophage foam cells via the ATP-binding cassette trans

110 C pneumoniae, frequently within macrophage foam cells, was identified in coronary fibrol

111 Macrophage foam cells were depleted in mPGES-1(-/-) LDLR

112 as elucidated a mechanism for development of macrophage foam cells when macrophages are incubated wit

113 osclerotic lesion is mediated by lipid-laden macrophages (foam cells), which also establish chronic i

114 capacity was quantified by incubating human macrophage foam cells with apoB-depleted serum.

115 ine was quantified using incubation of human macrophage foam cells with apolipoprotein B-depleted pla

116 poprotein, a key event in the development of macrophage foam cells within atherosclerotic lesions.

117 Furthermore, macrophage foam cells within lesions of the IL-10 Tg gro

118 facilitates cellular cholesterol efflux from macrophage foam cells within the intima of the lesion.