ライフサイエンスコーパス: foam cell

1 ons after co-culture with macrophage-derived foam cells).

2 a newly characterized pathway in macrophage foam cells.

3 through the formation of macrophage-derived foam cells.

4 Hb), are devoid of neutral lipids typical of foam cells.

5 atory-response genes, observed in macrophage foam cells.

6 Eventually, they ingest lipids and become foam cells.

7 ated glucose uptake in human macrophages and foam cells.

8 inocytosis converting these macrophages into foam cells.

9 by macrophages converts the macrophages into foam cells.

10 phagocytosis and efferocytosis in macrophage foam cells.

11 good potency on cholesterol efflux in THP-1 foam cells.

12 ecause it did not transform macrophages into foam cells.

13 mation of lipid-laden THP-1 macrophages into foam cells.

14 nsformation of macrophages into E-LDL-loaded foam cells.

15 promoting cholesterol efflux from macrophage foam cells.

16 ficantly higher numbers of viable macrophage foam cells.

17 of the myocardium and spleen with macrophage foam cells.

18 reby promoting the formation of inflammatory foam cells.

19 subendothelial space and differentiate into foam cells.

20 lated cholesterol is removed from macrophage foam cells.

21 o promote cholesterol efflux from macrophage foam cells.

22 y lipoproteins (LDLs), generating macrophage foam cells.

23 efficient to promote the formation of hVSMC foam cells, a crucial vascular component determining the

24 , the hyperlipidemic mice exhibited numerous foam cells, a probable cause of increased swelling and p

25 ge IGF1R signaling suppresses macrophage and foam cell accumulation in lesions and reduces plaque vul

26 but rather induced a significant macrophage foam cell accumulation in murine atherosclerotic plaques

27 ne deletion not only conferred protection to foam cells against H2O2-induced death but also switched

28 with respect to cholesterol efflux in THP-1 foam cells, albeit weaker in potency.

29 accumulation in macrophages and formation of foam cells, an early step in the development of atherosc

30 In vivo and in vitro foam cell analyses showed apoE-CD16 DKO macrophages accu

31 We previously proposed a mechanism involving foam cell anchorage to vascular smooth muscle cells beca

32 iate into macrophages and macrophage-derived foam cells and cause atherosclerotic lesions.

33 ly associated with cardiovascular disease in foam cells and clinical specimens from patients with AS.

34 ys-Ala-Gly-OH (Pam) became Oil Red O-stained foam cells and showed increased cholesteryl ester (CE) c

35 leukocyte accumulation, lipid accumulation, foam cells, and endothelial cell injury.

36 ent hyperlipidemic mice revealed accelerated foam-cell apoptosis, which subsequently led to the atten

37 yperlipidemic atherosclerosis by suppressing foam-cell apoptosis.

38 Foam cells are a hallmark of atherosclerosis.

39 Inflammation and macrophage foam cells are characteristic features of atheroscleroti

40 tes, from which macrophages and most DCs and foam cells are derived, and reduce atherosclerotic lesio

41 mouse and human atherosclerotic lesions; 2) foam cells are reduced in lesions in cx3cr1(-/-)apoE(-/-

42 Monocyte-derived foam cells are the hallmark of early atherosclerosis, an

43 Macrophage-derived foam cells are thought to play a major role in atheroscl

44 Lipid-laden macrophages or "foam cells" are the primary components of the fatty stre

45 er ischemic injury, less swelling, and fewer foam cells at 3 d after ischemia.

46 open new avenues for an innovative anti-VSMC foam cell-based strategy for the treatment of vascular l

47 alveolar macrophages and macrophage-derived foam cells, both cell types relevant to tuberculosis pat

48 humans, whereas inflammatory macrophages and foam cells, but not circulating monocytes, are major leu

49 promotes cholesterol efflux from macrophage foam cells by directly up-regulating its key cellular me

50 to the plaque and impaired the formation of foam cells by enhancing cholesterol efflux from macropha

51 e may facilitate the formation of macrophage foam cells by impairing cholesterol efflux by the ABCA1

52 s in macrophages and its transformation into foam cells by increasing the expression of scavenger rec

53 ich necroptosis was induced in THP-1-derived foam cells by serum deprivation.

54 on of cholesteryl esters (CEs) in macrophage foam cells, central to atherosclerotic plaque formation,

55 que size decreased by approximately 40%, and foam cell content by approximately 75%.

56 CR7 ligands CCL19 and CCL21, lesion size and foam cell content were substantially preserved.

57 In contrast, the size, foam cell content, and aortic pool size of iodinated LDL

58 oprotein (LDL) cholesterol-loaded macrophage foam cells contributes to the development of atheroscler

59 macrophages exhibit increased expression of foam cell differentiation markers including 15-lipoxygen

60 o promote cholesterol efflux from macrophage foam cells, direct experimental support for this hypothe

61 ony stimulating factor in splenic macrophage foam cells, driving BM monocyte and neutrophil productio

62 The varied behaviour of macrophages and foam cells during atherosclerosis and its clinical seque

63 In summary, in foam cells during atherosclerosis regression, there is i

64 n of excess cholesterol, as well as improves foam cell efferocytic function.

65 Cellular lipid efflux and foam cell emigration can occur surprisingly rapidly once

66 Lipid efflux and foam cell emigration each involve specific molecular med

67 ns (e.g. collagen, elastin) and lipids (e.g. foam cells, extracellular lipids) in the first 200 mum o

68 ids from plaques, and emigration of lesional foam cells followed by entry of healthy phagocytes that

69 toneal model of foam cell formation in which foam cells form in vivo independently of the model ligan

70 These findings correlated with decreased foam cell formation (2.27+/-0.57 versus 4.10+/-0.3; P<0.

71 , compared with vehicle control) and reduced foam cell formation (approximately 75%).

72 s a potential mechanism underlying increased foam cell formation and accelerated cardiovascular disea

73 pathways to identify regulators that control foam cell formation and atherogenesis.

74 king lipoprotein internalization will reduce foam cell formation and atherogenesis.

75 ts and is known to be involved in macrophage foam cell formation and atherosclerosis.

76 take in macrophages that would contribute to foam cell formation and atherosclerosis.

77 om macrophages, thereby reducing the risk of foam cell formation and atherosclerosis.

78 droplet protein (LDP), in the regulation of foam cell formation and atherosclerosis.

79 study investigated a novel role for Stat1 in foam cell formation and atherosclerosis.

80 ation antagonizes this program, resulting in foam cell formation and atherosclerosis; however, the mo

81 choline diet-enhanced endogenous macrophage foam cell formation and atherosclerotic lesion developme

82 ro, stat1 deficiency significantly inhibited foam cell formation and CD36 expression.

83 Macrophage foam cell formation and cholesterol efflux, together wit

84 macrophages may be an important mechanism of foam cell formation and contributor to atherosclerosis d

85 d an M2-predominant phenotype with increased foam cell formation and ER stress.

86 at could prevent both lipid accumulation and foam cell formation and further minimise the possible da

87 xtacrine responses associated with increased foam cell formation and inflammatory cytokine elaboratio

88 HLP showed potential in reducing foam cell formation and intracellular lipid accumulation

89 determined by assessing lipid accumulation, foam cell formation and JNK activation in wt, cd9 null a

90 nt of atherosclerosis, in part, by mediating foam cell formation and macrophage chemotaxis.

91 -mediated pathway for linked protection from foam cell formation and oxidant stress may have therapeu

92 data reveal novel signaling requirements for foam cell formation and suggest that uptake of distinct

93 by oxidized low-density lipoprotein promotes foam cell formation and the progression of atheroscleros

94 ntribution of Vav proteins to CD36-dependent foam cell formation and to identify the mechanisms by wh

95 ogenitor cell expansion and differentiation, foam cell formation and vascular inflammation.

96 hip between ER stress and macrophage-derived foam cell formation and whether ER stress would be invol

97 reviously thought, alternative mechanisms of foam cell formation are now being explored.

98 thways that link innate immune activation to foam cell formation are still poorly identified.

99 scued the suppression of CD36 expression and foam cell formation arising from Plg deficiency.

100 6) accumulate in vivo and mediate macrophage foam cell formation as well as promote platelet hyper-re

101 in mouse macrophages significantly inhibited foam cell formation assessed by lipid staining and chole

102 Foam cell formation because of excessive accumulation of

103 amma in the induction of CD36 expression and foam cell formation by 15(S)-HETE.

104 Next, we investigated foam cell formation by CRP-bound E-LDL.

105 t ANGPTL4 deficiency in macrophages promotes foam cell formation by enhancing CD36 expression and red

106 an M1 phenotype and subsequently suppressed foam cell formation by increasing HDL- and apoA-1-induce

107 ontaining adapter inducing IFN-beta promoted foam cell formation by inducing both NF-kappaB signaling

108 lation into M2 macrophages lead to increased foam cell formation by inducing scavenger receptor CD36

109 1,25(OH)(2)D(3) suppressed foam cell formation by reducing acetylated or oxidized l

110 ctive role during atherosclerosis-associated foam cell formation by signaling through the miR-155-CAR

111 ogenic cytokine TGF-beta inhibits macrophage foam cell formation by suppressing the expression of key

112 al role in CD36 up-regulation, enhancing the foam cell formation by uptaking more ox-LDL.

113 oduction and T cell activation, showing that foam cell formation can occur by immunosuppressive MP.

114 The Plg-dependent CD36 expression and foam cell formation depended on conversion of Plg to pla

115 This mechanism of macrophage foam cell formation does not depend on LDL modification

116 No role for LKB1 in foam cell formation has previously been reported.

117 These MP also stimulated foam cell formation in a human skin model.

118 diated oxidation, and its ability to prevent foam cell formation in a model for oxidised low density

119 grin activation controls CD36 expression and foam cell formation in alternatively activated monocyte/

120 Reduced foam cell formation in apoE-CD16 DKO mice is not due to

121 n-regulate CD36 expression and CD36-mediated foam cell formation in IL-13-stimulated monocytes/macrop

122 ion of liver X receptor dramatically reduced foam cell formation in macrophages from patients with ty

123 Stat1 regulates CD36 expression and foam cell formation in macrophages in vitro; the Stat1 r

124 which secrete cytokines that in turn enhance foam cell formation in macrophages.

125 ransgenic animals exhibit reduced macrophage foam cell formation in the arterial wall when these tran

126 Inflammatory processes accompany Mvarphi foam cell formation in the artery wall, yet the relation

127 tes reverse cholesterol transport and limits foam cell formation in THP-1 macrophages.

128 fferentiation (CD)36 expression with reduced foam cell formation in TR4(-/-) mice.

129 that decreased ABCG1 function can facilitate foam cell formation in Type 2 diabetic mice.

130 uptake of oxidized LDL (oxLDL) in vitro and foam cell formation in vitro and in vivo was significant

131 CD36-dependent uptake of oxLDL in vitro and foam cell formation in vitro and in vivo was significant

132 ration, differentiation into macrophages and foam cell formation in vitro and in vivo.

133 ced uptake of native LDL ex vivo and reduced foam cell formation in vivo, whereas sortilin overexpres

134 cytosis of LDL is a mechanism for macrophage foam cell formation in vivo.

135 In an intraperitoneal model of foam cell formation in which foam cells form in vivo ind

136 umoniae induced IRF3 activation and promoted foam cell formation in wild-type macrophages, whereas th

137 crophages from diabetic patients accelerated foam cell formation induced by modified LDL.

138 We show that ADFP expression facilitates foam cell formation induced by modified lipoproteins in

139 : (i) oxLDL binding to CD36, (ii) macrophage foam cell formation induced by oxLDL, and (iii) platelet

140 ith PPAR-delta agonists was shown to inhibit foam cell formation induced excessive levels of VLDL rem

141 We and others have shown that foam cell formation initiated by exposing macrophages to

142 Foam cell formation is a hallmark event during atheroscl

143 nd cellular processes that govern macrophage foam cell formation is critical to understanding the bas

144 In atherogenesis, macrophage foam cell formation is modulated by pathways involving b

145 red cholesterol suggests that the process of foam cell formation is not necessarily detrimental as lo

146 rogenic forms of LDL, but the role of CRP in foam cell formation is unclear.

147 mouse macrophages removed any dependency of foam cell formation on Stat1.

148 However, it is unclear whether foam cell formation per se protects against atherosclero

149 ing, their role in CD36-dependent macrophage foam cell formation remains unknown.

150 acrophages in vitro; the Stat1 regulation of foam cell formation requires CD36.

151 ved that M-CSF itself is capable of inducing foam cell formation similar to that seen in PAP.

152 holesterol accumulation mimicking macrophage foam cell formation that occurs within atherosclerotic p

153 MC1-R confers protection against macrophage foam cell formation through a dual mechanism: It prevent

154 yte/macrophage proinflammatory responses and foam cell formation through coordinated and combined act

155 We conclude that C. pneumoniae facilitates foam cell formation via activation of both MyD88-depende

156 that Vav proteins regulate oxLDL uptake and foam cell formation via calcium- and dynamin 2-dependent

157 protection via heme oxygenase 1 and reduced foam cell formation via liver X receptor, a potent combi

158 mportant role for KLF2 in primary macrophage foam cell formation via the potential regulation of the

159 Foam cell formation was associated with significant chan

160 Foam cell formation was diminished in FASKOM as compared

161 C. pneumoniae-induced foam cell formation was significantly reduced by the LXR

162 The mechanism of Stat1 regulation of foam cell formation was uniquely dependent on the scaven

163 and interleukin 6 (IL-6), and (3) increased foam cell formation when treated with oxLDL, attributabl

164 diet and LDL receptor genotype on macrophage foam cell formation within the peritoneal cavities of mi

165 intracellular cholesterol accumulation (ie, foam cell formation) and inflammasome activation, the ex

166 Chlamydia pneumoniae induces macrophage foam cell formation, a hallmark of early atherosclerosis

167 modified low-density lipoprotein uptake and foam cell formation, all of which were abolished by bloc

168 fect of air pollution on 7-KCh accumulation, foam cell formation, and atherosclerosis.

169 rosclerosis, decreased peritoneal macrophage foam cell formation, and downregulated ER stress protein

170 OxLDL uptake, lipid accumulation, foam cell formation, and JNK phosphorylation were partia

171 c lipid droplets is a hallmark of macrophage foam cell formation, and the molecular basics involved i

172 n Apoe(-/-) mice led to in vivo increases in foam cell formation, aortic 25-HC levels, and disease pr

173 ation, endothelial cell function, macrophage foam cell formation, as well as insulin secretion from p

174 ake of OxLDL by macrophage SR contributes to foam cell formation, but the importance of this pathway

175 ng cascades that are required for macrophage foam cell formation, but the mechanisms by which CD36 si

176 oxidized low density lipoprotein uptake, and foam cell formation, critical events underlying the path

177 ve the capacity to regulate inflammation and foam cell formation, pathological angiogenesis and calci

178 neutralizing and clearing OSE and preventing foam cell formation, suggesting similar applications in

179 ncy of lysosomal phospholipase A2 results in foam cell formation, surfactant lipid accumulation, sple

180 aining plasma lipoproteins lead to increased foam cell formation, the first step in the development o

181 butions of lipid uptake and TLR signaling in foam cell formation, we established an in vitro assay us

182 3-induced CD36 expression and CD36-dependent foam cell formation, whereas13(S) Hydroperoxyoctadecadie

183 We found that lipid-containing MP promoted foam cell formation, which was enhanced by TLR stimulati

184 otal role of plasminogen (Plg) in regulating foam cell formation.

185 sterol ester accumulation in macrophages and foam cell formation.

186 IFN-alpha to TLR2 activator promoted robust foam cell formation.

187 ogenous microparticles (MP) to contribute to foam cell formation.

188 ich is a counterregulatory mechanism against foam cell formation.

189 tivation of multiple distinct TLR can induce foam cell formation.

190 ansport in macrophages, which contributes to foam cell formation.

191 rotein (oxLDL) by macrophages (Mvarphis) and foam cell formation.

192 aintaining chronic inflammation and inducing foam cell formation.

193 roliferator-activated receptor alpha blocked foam cell formation.

194 vel macrophage subset that is protected from foam cell formation.

195 droxycholesterol (25-HC) promotes macrophage foam cell formation.

196 ted that the TF ATF3 may regulate macrophage foam cell formation.

197 o not induce IFN, like TLR2, did not enhance foam cell formation.

198 a signaling pathway required for macrophage foam cell formation.

199 protein expression, as well as CD36-related foam cell formation.

200 y which Vav proteins regulate CD36-dependent foam cell formation.

201 nted macrophage cholesterol accumulation and foam cell formation.

202 ificantly blocked oxLDL uptake and inhibited foam cell formation.

203 lipid bodies in macrophages and consequently foam cell formation.

204 MAC mediated endothelial damage and promoted foam cell formation.

205 CD36 expression with decreased or increased foam cell formation.

206 down macrophage cells reversed the decreased foam cell formation.

207 development of atherosclerosis is macrophage foam cell formation.

208 ce or absence of oxidized LDL, then measured foam cell formation.

209 ux and hence play a vital role in macrophage foam cell formation.

210 or IRF3, but not TLR3, significantly reduced foam cell formation.

211 stablish the role of LKB1 in atherosclerotic foam cell formation.

212 rs to be a relatively pure model of impaired foam cell formation.

213 cholesterol efflux, and increased macrophage foam cell formation.

214 es monocyte differentiation, activation, and foam cell formation.

215 by modulating cellular processes involved in foam cell formation.

216 ol LDLR(-/-) mice, using an in vivo model of foam cell formation.

217 ophages resulted in increased LDL uptake and foam cell formation.

218 rosis and we demonstrated a role for 25HC in foam cell formation.

219 onses to inflammatory signals, and increased foam cell formation.

220 ar function, reduce inflammation and inhibit foam cell formation.

221 is, centered on the regulation of macrophage foam cell formation.

222 had decreased CD36 expression and diminished foam cell formation.

223 signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and finding

224 Thus, macrophage Hilpda is crucial to foam-cell formation and lipid deposition, and to control

225 cing atherosclerosis progression by inducing foam-cell formation, metabolic adaptation of infiltrated

226 A1 recognition, cholesterol accumulation and foam-cell formation.

227 show that MafB is predominantly expressed in foam cells found within atherosclerotic lesions, where M

228 y xanthoma cells (lipid-laden macrophages or foam cells) found in the superficial connective tissue.

229 D68(+), primarily macrophages and macrophage foam cells) from plaques.

230 To characterize these foam cells further, immunohistochemical techniques were

231 leukocyte accumulation, lipid accumulation, foam cell generation and endothelial cell injury were al

232 d ability to promote cholesterol efflux from foam cells in an ABCG1-dependent pathway due to an incre

233 mice reduces the number of lipid droplets in foam cells in atherosclerotic lesions and protects the m

234 of SMPDL3A by cholesterol-loaded macrophage foam cells in lesions may decrease local concentrations

235 ein Nef causes dyslipidemia and formation of foam cells in mouse models of atherosclerosis.

236 otein degradation and uptake into macrophage foam cells in the arterial intima.

237 promotes cholesterol efflux from macrophage foam cells in the arterial wall.

238 subsequent accumulation of leukocyte-derived foam cells in the artery wall.

239 y accepting free cholesterol from macrophage foam cells in the artery wall.

240 iltration, thereby stimulating regression of foam cells in the artery.

241 D68+ macrophages, including lipid-containing foam cells, in atherosclerotic lesions in the aortic arc

242 ulture of large SMCs with macrophage-derived foam cells induced a transition to the small phenotype w

243 Foam cell infiltration was responsible for 70% of false

244 ferentiation of macrophages into lipid-laden foam cells is central to the development of atherosclero

245 cholesterol efflux capacity from macrophage foam cells is not associated with cardiovascular or all-

246 age phenotype, but how this is controlled in foam cells is not known.

247 erogenesis because their transformation into foam cells is responsible for deposition of lipids in pl

248 accumulation and the consequent formation of foam cell-like cells in adipose tissue.

249 Macrophages, DCs, foam cells, lymphocytes, and other inflammatory cells ar

250 n mediating cellular cholesterol efflux from foam cell macrophages and to identify the cellular chole

251 Cholesterol-loaded foam cell macrophages are prominent in atherosclerotic l

252 emplified by the requirement of lipid-laden, foam cell macrophages for atherosclerotic lesion formati

253 the function of CRP to prevent formation of foam cells may influence the process of atherogenesis.

254 pients, there were 3- to 6-fold increases in foam cells of mRNA for liver X receptor alpha and choles

255 s affected cholesterol-ester accumulation in foam cells of the THP1 monocytic cell line.

256 ine consistent marker sets for the different foam cell phenotypes in experimental animals and humans.

257 further demonstrate activation of macrophage/foam cell PI3-kinase/Akt in atherosclerotic plaques from

258 e relative contribution of SMCs to the total foam cell population and their expression of ABCA1 in co

259 smooth muscle cells (SMCs) contribute to the foam cell population in arterial plaque, and express low

260 rogression of macrophages to the lipid-laden foam cells present in atherosclerotic plaques.

261 Macrophage-derived foam cells promote selective migration from the media of

262 mation of lipid-laden macrophages, known as "foam cells." Recently, we reported that CD36, a scavenge

263 nd the SMC-specific marker SM alpha-actin of foam cell-rich lesions revealed that 50+/-7% (average+/-

264 LDL in the presence of C1q alters macrophage foam cell survival or function.

265 /-)LDLR(-/-) mice develop significantly more foam cells than control LDLR(-/-) mice, using an in vivo

266 -rich lipoprotein particles, and evolve into foam cells that form components of vulnerable atheroscle

267 ltiple roles for Prx I in macrophage-derived foam cells that include functionality as both an antioxi

268 Foam cells that stained positively with RM3/1, 25F9, and

269 ught to be a key process in the formation of foam cells, the hallmark of early atherosclerotic lesion

270 BM cleaves CD36 and reduced the formation of foam cells, the hallmark of M. tuberculosis infection.

271 Oxidized lipoproteins convert macrophages to foam cells through lipid uptake and TLR signaling.

272 and CX3CL1 mediate heterotypic anchorage of foam cells to CASMCs in the context of atherosclerosis a

273 Foam cell transformation of lipid-laden THP-1 macrophage

274 y role in IFN-gamma-induced inflammation and foam cell transformation, a better understanding of the

275 tivation and thereby regulates macrophage to foam cell transformation.

276 were dramatically suppressed in lipid-laden foam cells treated with IL10.

277 Foam cells undergo apoptosis and, if not efficiently cle

278 Macrophages transform into foam cells upon taking-in lipids.

279 n promote cholesterol efflux from macrophage foam cells via the ATP-binding cassette transporters ABC

280 The percentage of antibody-labeled foam cells was determined by visual counts of selected f

281 in eliminating the activity of E-LDL to form foam cells was not impaired by the presence of PEt.

282 them, we found that the level of miR-155 in foam cells was the most significantly elevated in a dose

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

284 In macrophages from TLR2(-/-) mice, foam cells were induced by Escherichia coli LPS but not

285 Foam cells were isolated by laser capture microdissectio

286 he diseased portion, only macrophage-derived foam cells were retrieved.

287 d error of the mean, n=14 subjects) of total foam cells were SMC derived.

288 bility to take up lipids and to develop into foam cells when exposed to modified low-density lipoprot

289 d migration and apoptosis of macrophages and foam cells, whereas TIMP-1 failed to exert similar effec

290 esterol efflux from human macrophage-derived foam cells, which is a critical factor of atherogenesis.

291 ated the caspase-3 and caspase-8 pathways in foam cells, which is responsible for the switch from nec

292 ty lipoprotein and [(3)H]cholesterol to form foam cells, which were then treated with apolipoprotein

293 as quantified by incubating human macrophage foam cells with apoB-depleted serum.

294 ntified using incubation of human macrophage foam cells with apolipoprotein B-depleted plasma.

295 internalize modified lipids, and convert to foam cells with diseased phenotypes.

296 e treated macrophages and macrophage-derived foam cells with exogenous TIMP-2 in vitro.

297 oneal macrophages revealed the appearance of foam cells with lamellar inclusion bodies, a hallmark of

298 ns contain primarily reparative and resident foam cells, with limited numbers of inflammatory macroph

299 after SCI, macrophages are best described as foam cells, with lipid catabolism representing the main

300 after SCI, macrophages are best described as foam cells, with lipid catabolism representing the main