ライフサイエンスコーパス: free cholesterol

1 s by increasing the availability of cellular free cholesterol.

2 crophages was considered the major source of free cholesterol.

3 glands from Lxralphabeta-/- mice accumulated free cholesterol.

4 lesterol is secreted into bile, primarily as free cholesterol.

5 o exhibited absence or dramatic reduction in free cholesterol.

6 due in part to the secondary accumulation of free cholesterol.

7 he pathways are involved in the secretion of free cholesterol.

8 ing the formation of cholesterol esters from free cholesterol.

9 sphingomyelin, which has a high affinity for free cholesterol.

10 n (HDL) cholesteryl esters and the efflux of free cholesterol.

11 polipoprotein B-100, phospholipids, and some free cholesterol.

12 incorporation of dipalmitoyl-PC, but not by free cholesterol.

13 ould be inhibited by replenishing cells with free cholesterol.

14 rhage with deposition of erythrocyte-derived free cholesterol.

15 sferases (ALT/AST) and hepatic triglycerides/free cholesterol.

16 e cholesterol but poorly with hepatic tissue free cholesterol.

17 absence of changes in the concentrations of free cholesterol.

18 Adipose harbors a large depot of free cholesterol.

19 ated at the SML equivalent of about 30 mol % free cholesterol.

20 olesterol oxidase-sensitive pool of membrane free cholesterol, 2) mediate cholesterol efflux to HDL,

21 differ significantly from those labeled with free cholesterol ((3)H-FC).

22 phospholipid (26%), cholesteryl ester (24%), free cholesterol (37%), and apoAI (22%).

23 crease in VLDL and LDL phospholipids (210%), free cholesterol (60%), and cholesteryl ester (40%) with

24 cholesterol (63%), cholesteryl ester (63%), free cholesterol (67%), non-high density lipoprotein (HD

25 l esters but does not play a primary role in free cholesterol absorption.

26 Investigating further, we found that free cholesterol accumulated in PMN lipid raft fractions

27 Free cholesterol accumulated in the endoplasmic reticulu

28 cholesterol homeostasis causes intracellular free cholesterol accumulation and hepatocyte injury.

29 ccumulation in lysosomal storage disease and free cholesterol accumulation in cell membranes in ather

30 the capacity of glucolipotoxicity to induce free cholesterol accumulation in human pancreatic islets

31 f this phospholipid response to keep up with free cholesterol accumulation in lesional macrophages in

32 e domains but lacks the START domain, caused free cholesterol accumulation in lysosomes and inhibited

33 PC2 (progressive neurodegenerative symptoms, free cholesterol accumulation in lysosomes).

34 and MBL also significantly reduced levels of free cholesterol accumulation in monocytes and human mon

35 m macrophages to protect against toxicity of free cholesterol accumulation in the cell.

36 ged Sort1 knock-out mice showed less hepatic free cholesterol accumulation, increased bile acid synth

37 itive endocytic recycling compartment, where free cholesterol also accumulated as revealed by filipin

38 macrophages with 7-ketocholesterol, but not free cholesterol, also inhibited expression of SR-BI.

39 th Abeta and submicromolar concentrations of free cholesterol alter the trafficking of a population o

40 terol ester concentrations and reductions in free cholesterol amounts.

41 Compared with baseline values, serum free cholesterol, an index of tissue cholesterol mobiliz

42 a [(3)H]benzophenone-modified photoactivable free cholesterol analogue ((3)H-FCBP) did not differ sig

43 ncreased proportion of total plasma, and HDL free cholesterol and a marked (>10-fold) reduction in mo

44 ed blood cell membranes are a rich source of free cholesterol and accumulated red blood cells within

45 ree fatty acids, esterified cholesterol, and free cholesterol and also a much higher content of satur

46 etion is tightly coupled to the secretion of free cholesterol and bile salts.

47 oading-induced intracellular accumulation of free cholesterol and cholesterol esters in macrophages.

48 ycin decreased intracellular accumulation of free cholesterol and cholesterol esters induced by the e

49 d intracellular accumulation of cholesterol (free cholesterol and cholesterol esters), whereas activa

50 ylated lipid and Pry1 and Pry2 proteins bind free cholesterol and cholesteryl acetate in vitro.

51 /-)-->LDLr(-/-) mice had significantly lower free cholesterol and cholesteryl ester levels in the bra

52 ty of the polar lipids, but left significant free cholesterol and fatty acids, and small but critical

53 in NPC disease exhibit extensive storage of free cholesterol and glycosphingolipids (GSLs), includin

54 ptor signaling by reducing cellular membrane free cholesterol and lipid raft content, indicating a ro

55 iated through alterations in plasma membrane free cholesterol and lipid raft content.

56 rhage into the necrotic core are a source of free cholesterol and may become a driving force in the p

57 Two analogues (1, 2) of free cholesterol and one analogue (3) of the immunosuppr

58 caveolin expression is regulated by cellular free cholesterol and plasma levels of low-density lipopr

59 c potential, to prevent the increase in both free cholesterol and ROS levels induced by glucolipotoxi

60 facilitation of the intestinal absorption of free cholesterol and the modification of plasma lipoprot

61 t reagentless biosensor for determination of free cholesterol and total cholesterol has been realized

62 cm(-2) and 760 microA mM(-1) cm(-2) towards free cholesterol and total cholesterol respectively with

63 mitoyl-2-oleoyl-sn-glycero-3-phosphocholine, free cholesterol, and apoA-I.

64 e loss of large HDL particles, increased HDL-free cholesterol, and decreased HDL protein in CBS(-/-)/

65 ation of intraplaque hemorrhage, accumulated free cholesterol, and necrotic core expansion is beginni

66 iglycerides, with less definite ones between free cholesterol, and phospholipids for a specific group

67 lipoprotein (HDL) composed of phospholipid, free cholesterol, and protein, primarily apoE and apoJ.

68 by negative-stain electron microscopy of the free cholesterol- and phospholipid-enriched IDL/LDL frac

69 f CE and a surface enriched in phospholipid, free cholesterol, apoA-II, and apoE.

70 As expected, increases in hepatic free cholesterol are associated with decreases in 3-hydr

71 cells in atherosclerotic lesions accumulate free cholesterol as well as cholesteryl ester.

72 phospholipids, L-HDL cholesterol, and L-HDL-free cholesterol, as well as HDL cholesterol seem to be

73 smembrane pore depend on the availability of free cholesterol at the membrane surface, while changes

74 Free cholesterol at very low concentrations regulated Ca

75 R stress correlates strongly with hepatic ER free cholesterol but poorly with hepatic tissue free cho

76 of function was shown to lower intracellular free cholesterol, causing upregulation of HMG Co-A reduc

77 in selective cholesteryl ester uptake and in free cholesterol cellular efflux.

78 Triglyceride, free cholesterol, cholesterol ester, and phospholipid co

79 combination of effects directed by elevated free cholesterol, cholesterol esters and cholic acid, an

80 ucose or 1-[(14)C]acetate incorporation into free cholesterol, cholesterol esters, triglycerides, fre

81 a mechanism whereby the elevation of hepatic free cholesterol concentrations by dietary cholesterol,

82 lgus monkeys but not in green monkeys, liver free cholesterol concentrations were elevated when chole

83 lungs, accompanied with decreased pulmonary free cholesterol content and suppressed tumor cell proli

84 m ABCA1(-A/-A) mice had a 2-fold increase in free cholesterol content compared with wild-type mice an

85 C transfer by PLTP decreases with increasing free cholesterol content in rHDL and with decreasing HDL

86 Total and free cholesterol content was significantly higher in 25

87 n direct correlation with increased cellular free cholesterol content.

88 ncluding free fatty acid toxicity, increased free cholesterol, cytokine-mediated injury and activatio

89 d inflammation may therefore in part reflect free cholesterol- dependent changes in lipid raft struct

90 F expression was equally sufficient to cause free cholesterol-dependent apoptosis in podocytes by act

91 TNF-stimulated free cholesterol-dependent apoptosis in podocytes was me

92 sm in which local TNF is sufficient to cause free cholesterol-dependent podocyte injury irrespective

93 l pool in J774-SRBI cells, suggests that the free cholesterol derived from the hydrolysis of choleste

94 -) astrocytes secrete little phospholipid or free cholesterol despite comparable apoJ expression, sug

95 of free cholesterol transport, and modulates free cholesterol distribution between the plasma membran

96 ified cholesterol but did not reduce hepatic free cholesterol due to a compensatory increase in the r

97 holesteryl esters (CEs) and thereby enhances free cholesterol efflux and reduces cellular CE content.

98 ABCA1 facilitates free cholesterol efflux from peripheral tissues.

99 Free cholesterol efflux to HDL was increased ( approxima

100 Indeed, beyond its role in mediating free cholesterol efflux to HDL, the ABCG1 transporter eq

101 These studies suggest that free cholesterol enrichment of either plasma or endosoma

102 Renal cortical-free cholesterol (FC) and cholesterol ester (CE) levels

103 es indicate that acute tubular injury causes free cholesterol (FC) and cholesteryl ester (CE) accumul

104 Using gas chromatographic analysis, free cholesterol (FC) and esterified cholesterol (CE) we

105 to apoA-I, and had a significant increase in free cholesterol (FC) and membrane lipid rafts without i

106 in atherosclerotic lesions accumulate excess free cholesterol (FC) and phospholipid.

107 phages in atherosclerotic lesions accumulate free cholesterol (FC) as well as cholesteryl ester and a

108 ing stimulation of the bidirectional flux of free cholesterol (FC) between cells and HDL and changes

109 SR-BI stimulates the bi-directional flux of free cholesterol (FC) between cells and lipoproteins, an

110 (SR-BI) stimulates the bidirectional flux of free cholesterol (FC) between HDL and SR-BI-expressing c

111 tein (HDL) cholesteryl ester, stimulation of free cholesterol (FC) efflux from cells to HDL and phosp

112 unregulated, extracellular acceptor-mediated free cholesterol (FC) efflux is rate limited by the intr

113 Phospholipid (PL) and free cholesterol (FC) efflux maintain homeostasis.

114 By promoting cellular free cholesterol (FC) efflux, HDL and its apolipoprotein

115 dividing cells during S-phase, together with free cholesterol (FC) efflux.

116 ow-density lipoprotein (LDL) reduced CER (1% free cholesterol (FC) esterified/h) compared to B6 (6% F

117 There is increasing interest in cellular free cholesterol (FC) excess as an inducer of lesional m

118 that scavenger receptor BI (SR-BI) promotes free cholesterol (FC) exchange between high density lipo

119 g, selective uptake of HDL-CE and release of free cholesterol (FC) from cells to HDL.

120 yers, an increase in the selective uptake of free cholesterol (FC) from plasma low density lipoprotei

121 After removal of inhibitor, free cholesterol (FC) homeostasis was determined at inte

122 cause of macrophage death is accumulation of free cholesterol (FC) in the ER, leading to activation o

123 give rHDL increases as the level of membrane free cholesterol (FC) increases up to 20 mol % when the

124 Free cholesterol (FC) is selectively internalized from l

125 atively direct effects of ceramide (Cer) and free cholesterol (FC) on meibomian lipid films (MLF) usi

126 erminus for a major pathway of intracellular free cholesterol (FC) transport.

127 lphosphatidylcholine (POPC) with and without free cholesterol (FC) was studied by isothermal titratio

128 diacylglycerol (DAG), triacylglycerol (TAG), free cholesterol (FC), cholesterol ester, and phospholip

129 Isolation of free cholesterol (FC), cholesteryl ester (CE), and trigl

130 eath is intracellular accumulation of excess free cholesterol (FC), which is known to occur in vivo.

131 LCAT bound to (3)H-free cholesterol (FC)-labeled pre-beta(1)-HDL generated

132 as inactive in binding phospholipids (PL) or free cholesterol (FC).

133 raphy (FPLC) after radiolabeling with [(3)H]-free cholesterol (FC).

134 hydrolyzed by liposomal lipases to generate free cholesterol (FC).

135 d SU by FFA was secondary to changes in cell-free cholesterol (FC).

136 accumulate large amounts of unesterified or "free" cholesterol (FC), a process that is thought to con

137 A1-mediated efflux of cellular unesterified (free) cholesterol (FC) and phospholipid (PL) is not well

138 poA-I modification on cellular unesterified (free) cholesterol (FC) efflux, three recombinant human a

139 (PC), sphingomyelin (SM), and unesterified (free) cholesterol (FC) from J774 macrophages, in which A

140 Unesterified, or "free," cholesterol (FC) is a potent inducer of macrophag

141 nd macrophages with excess unesterified, or "free," cholesterol (FC).

142 ccumulate large amounts of unesterified, or "free," cholesterol (FC).

143 ds, peptide cross-linked by photoactivatable free cholesterol (FCBP)], (iv) selectivity for interacti

144 We conclude that SR-BI-mediated free cholesterol flux is highly sensitive to HDL phospho

145 id in scavenger receptor BI (SR-BI)-mediated free cholesterol flux was examined by manipulating HDL(3

146 L phospholipid composition on SR-BI-mediated free cholesterol flux were not correlated with changes i

147 roles for serum albumin and erythrocytes in free cholesterol flux.

148 glycerides, wax esters, squalene, ceramides, free cholesterol, free fatty acids, and cholesterol and

149 y in organs predisposed to the extraction of free cholesterol from bilayers, such as the skin, lung,

150 o disruption may involve the accumulation of free cholesterol from erythrocyte membranes.

151 We also found rapid in vivo transfer of free cholesterol from HDL to apoB-lipoproteins in ABCA1-

152 otects against vascular disease by accepting free cholesterol from macrophage foam cells in the arter

153 The clearance of free cholesterol from plasma lipoproteins by tissues is

154 s storage is accompanied by sequestration of free cholesterol in a manner similar to that observed in

155 nhancing ACAT activity, reduce the amount of free cholesterol in a putative regulatory pool that feed

156 Glucolipotoxicity treatment increased free cholesterol in beta-cells, which was accompanied by

157 lytical performance for the determination of free cholesterol in human serum samples.

158 ol esterification, cause the accumulation of free cholesterol in intracellular membranes, deplete end

159 mbosis, whereas their macrophages accumulate free cholesterol in late endosomes and show increased ca

160 known coregulation and association of SM and free cholesterol in lipid rafts.

161 ed the accumulation of cholesteryl ester and free cholesterol in liver that was induced under the var

162 in enhanced oxidative damage, and increased free cholesterol in liver under stress accompanied by lo

163 umulation of low density lipoprotein-derived free cholesterol in lysosomes, is caused by mutations in

164 activated in response to the accumulation of free cholesterol in macrophages.

165 able to discriminate between esterified and free cholesterol in milk.

166 a and LXRbeta) in preventing accumulation of free cholesterol in mouse adrenal glands by controlling

167 terification and changes the distribution of free cholesterol in neurons.

168 ld-type and M 19 CHO cells, with most of the free cholesterol in normal and mutant CHO cells located

169 f intraplaque hemorrhage as a contributor of free cholesterol in plaques and point to its provocative

170 Free cholesterol in plaques is an emerging contributing

171 Quantitative analysis of free cholesterol in serum using reactive DESI was demons

172 perlipidemia can lead to the accumulation of free cholesterol in the artery wall, and that this promo

173 se element reporter assay, we confirmed that free cholesterol in the ER was also reciprocally modulat

174 We find that accumulation of free cholesterol in the late endosomes/lysosomes of Arf6

175 MTP reduces cholesteryl esters and enhances free cholesterol in the liver and intestine without dimi

176 ed to be much less toxic than the buildup of free cholesterol in the lysosomes of patients with mutat

177 than 100 fold less than the exchange rate of free cholesterol in the same conditions.

178 apoA-I-/- mice, promoted the accumulation of free cholesterol in the very low-density lipoprotein (VL

179 ed hypertriglyceridemia, the accumulation of free cholesterol in VLDL and HDL, and the formation of d

180 Several lines of evidence demonstrated that free-cholesterol-induced autophagy, which led to increas

181 esterol that could increase the partition of free cholesterol into membranes.

182 o equilibrate, indicating that bulk cellular free cholesterol is isolated from that participating in

183 An increase in free cholesterol is observed in aggregates contained in

184 tals to which recycling or newly synthesized free cholesterol is transported prior to efflux or redis

185 Free cholesterol is very efficiently removed from cells

186 sition of natural HDL and, importantly, bind free cholesterol (K(d) = 4 nM).

187 cyl groups from phospholipids to the 3-OH of free cholesterol, leading to the removal of excess chole

188 y, ACAT-1 inhibition increased intracellular free cholesterol level, which was associated with elevat

189 Treatments that change cellular free cholesterol levels also modulate the trafficking of

190 Increased extracellular free cholesterol levels are toxic to neurons; this toxic

191 ly LXRalpha provides a safety valve to limit free cholesterol levels as a basal protective mechanism

192 tudies have shown that increases in cellular free cholesterol levels stimulate apoE transcription in

193 lls showed significant reduction in cellular free cholesterol levels, with no cytotoxicity up to 5 mi

194 anism to avoid toxicity associated with high free cholesterol levels.

195 hese observations, we fed TNFalpha-secreting free cholesterol-loaded apoptotic macrophages to a healt

196 TNFalpha is released by free cholesterol-loaded apoptotic macrophages, and the c

197 StarD5 expression increased 3-fold in free cholesterol-loaded macrophages, which activate the

198 HDL reversed impaired chemotaxis in free cholesterol-loaded WT macrophages but was without e

199 age death, macrophages rendered apoptotic by free cholesterol loading (FC-AMs) were incubated briefly

200 ophages undergo ER stress and apoptosis upon free cholesterol loading (FCL).

201 In contrast free cholesterol loading of macrophages leads to imbalan

202 arious stimuli such as nutrient deprivation, free cholesterol loading, and oxidized LDL.

203 ring endoplasmic reticulum stress induced by free cholesterol loading.

204 ORMDL1 degradation was specific to free-cholesterol loading as autophagy induced by serum s

205 By contributing to the deposition of free cholesterol, macrophage infiltration, and enlargeme

206 rane of target cells is dictated by how much free cholesterol molecules are present.

207 that alpha-toxin may increase the number of free cholesterol molecules in the membrane.

208 reverse cholesterol transport by esterifying free cholesterol on HDL particles.

209 olesterol oxidase-sensitive pool of membrane free cholesterol on the other.

210 r, and ultimately into the bile and feces as free cholesterol or bile acids.

211 wed increased apoptosis when challenged with free cholesterol or oxidized LDL loading.

212 hages from apoptosis induced by loading with free cholesterol or oxidized LDL.

213 ree major branches of the UPR in response to free cholesterol or oxysterol loading in insulin-resista

214 reased apoptosis in response to loading with free cholesterol or oxysterol, but underlying mechanisms

215 ations in apoA-I(-/-) HDL particle diameter, free cholesterol or phospholipid content, or the apoE or

216 zyme 1beta, a combined reduction of cellular free cholesterol or triglyceride or both and MTP activit

217 Only traces of free cholesterol oxides were found (25-OH, 7-k, 7alpha-O

218 ble increase in cholesterol esters, although free cholesterol persisted at wild type levels, which mi

219 onstrating a direct relationship between the free cholesterol: phospholipid ratio and cellular necros

220 an adaptive response to prevent the cellular free cholesterol: phospholipid ratio from reaching cytot

221 lasma cholesterol, cholesteryl esters (CEs), free cholesterol, phospholipids, HDL cholesterol, and ap

222 bined with the measurement of the smaller ER free cholesterol pool in J774-SRBI cells, suggests that

223 though J774-SRBI cells manifested a smaller free cholesterol pool in the endoplasmic reticulum.

224 etains the membrane condensing properties of free cholesterol regardless of the chemistry or position

225 High-density lipoproteins, responsible for free cholesterol removal, are reduced in patients with i

226 Adipose tissue (AT) is the body's largest free cholesterol reservoir and abundantly expresses ATP

227 o chylomicrons, absorption of phospholipids, free cholesterol, retinol, and vitamin E also involves H

228 mained significantly higher than that of the free cholesterol, suggesting that cholesterol derived fr

229 e reduced macrophage immunostaining and more free cholesterol than control lesions.

230 ey molecules involved in the accumulation of free cholesterol that are selectively induced in high-ri

231 e membranes is their high relative levels of free cholesterol; the mole ratio of cholesterol to phosp

232 converted approximately 0.1-2% of total cell-free cholesterol to [14C]cholesteryl esters.

233 pression alters the distribution of membrane-free cholesterol to a caveolar fraction or alters the ac

234 The efflux of cellular phospholipid and free cholesterol to apolipoprotein A-I promoted by ABCA1

235 Although esterification of free cholesterol to cholesteryl ester in the liver is kn

236 CAT1 and ACAT2) are two enzymes that convert free cholesterol to cholesteryl esters.

237 The efflux of free cholesterol to HDL was the same in sense and antise

238 golipid, C8-lactosylceramide (C8-LacCer), or free cholesterol to human fibroblasts at 10 degrees C ca

239 The addition of free cholesterol to ldlA7-SRBI cells also stimulated cho

240 inositol, sphingomyelin, and partial loss of free cholesterol transfer activities.

241 The MLN64 START domain stimulated free cholesterol transfer from donor to acceptor mitocho

242 Almost all the free cholesterol transferred from lipoproteins to cells

243 Only 5% of the free cholesterol transferred to cells was esterified, in

244 f SR-BI in macrophages increases the rate of free cholesterol transport, and modulates free cholester

245 tive selective uptake rate constants for CE, free cholesterol, triglycerides (triolein), and phosphat

246 icking of these vesicles may be regulated by free cholesterol under physiological conditions.

247 s system for quick and reliable detection of free cholesterol using unaided eye.

248 The clearance of lysosomal free cholesterol was also associated with a decrease in

249 The absorption of free cholesterol was also not significantly different be

250 The reduction in cellular free cholesterol was associated with correction of abnor

251 ndent accumulation of cholesteryl esters and free cholesterol was detected in the plaques of the chol

252 essing GX sPLA(2) was reversed when cellular free cholesterol was normalized using cyclodextrin.

253 ive blue shade product depending on level of free cholesterol, when tested on complex system of human

254 creased the ratio of cholesterol esters over free cholesterol, whereas inhibition of p38 MAPK with SB

255 E levels, fewer lipid bodies, and accumulate free cholesterol, which causes injurious membrane effect

256 ABCA1)-mediated assembly of phospholipid and free cholesterol with apoA-I plays an important role in

257 components, i.e., XL-HDL cholesterol, XL-HDL-free cholesterol, XL-HDL phospholipids, L-HDL cholestero