ライフサイエンスコーパス: oxLDL

1 oxLDL activated RhoA and RhoA kinase (ROCK) to induce in

2 oxLDL also accumulated in the spleen.

3 oxLDL also induced rapid spreading and actin polymerizat

4 oxLDL increased cytosolic G protein by 350% in Chinese h

5 oxLDL is a potent pangenotype HCV entry inhibitor that m

6 oxLDL, but not native LDL, induced shape change, spreadi

7 oxLDL-induced impairment of endothelium-dependent vascul

8 oxLDL-induced ROS generation was blocked by the reduced

9 oxLDL-induced signaling events in human vascular endothe

10 lose proximity to zonula occludens-1 (ZO-1), oxLDL treatment induced a disorganization of JAM-C local

11 C, and triglycerides were mutually adjusted, oxLDL was no longer predictive.

12 HODE also did not affect oxLDL uptake.

13 mol HA-disaccharide/cell and increased after oxLDL treatment to 53.9 +/- 5.6.

14 bodies that bind not only bacteria, but also oxLDL.

15 Although oxLDL stimulates activatory signaling, it is unclear how

16 lls (HASMC) were found to express JAM-C, and oxLDL, as well as enzymatically modified LDL (eLDL) sign

17 and 166) failed to recognize oxPC(CD36) and oxLDL.

18 al role of adipose tissue in cholesterol and oxLDL metabolism remains to be established, the inductio

19 sociation with total and LDL cholesterol and oxLDL/LDL, not seen with PLA2G2A, thus confirming distin

20 The data suggest competition between FA and oxLDL for access to the CD36 binding pocket.

21 n a predicted CD36 binding domain for FA and oxLDL.

22 Although chemically different, L5 and oxLDL competed for EC entry through LOX-1.

23 rnalize approximately 12 to 16 pg of LDL and oxLDL in 24 hours.

24 ng the internalization mechanisms of LDL and oxLDL in vitro.

25 showed blunted internalization of oxLDL and oxLDL-induced inflammation.

26 e concentrations, on serum lipid profile and oxLDL of male Wistar rats fed a cholesterol-enriched die

27 and activator of transcription 3 in SS- and oxLDL-dependent manner.

28 Anti-oxLDL serum concentration-time profiles showed a biphasi

29 Anti-oxLDL was administered as a single intravenous (IV) dose

30 Anti-oxLDL was conjugated with the N-hydroxysuccinimide ester

31 containing or devoid of PC could absorb anti-oxLDL from human sera.

32 ation between the ratios of anti-PC and anti-oxLDL (Spearman's rho = 0.35, P = 0.0037), local product

33 The local production of anti-PC and anti-oxLDL further implicates the oral flora as a source of a

34 uld be able to detect local anti-PC and anti-oxLDL production in gingival crevicular fluid (GCF).

35 ligand binding assay that measured free anti-oxLDL (unbound and partially bound forms) and Assay B me

36 t of IgG anti-PC, IgG anti-LDL, and IgG anti-oxLDL by enzyme-linked immunosorbent assay.

37 Immunization with pneumococci increased anti-oxLDL IgM levels and led to a reduction in hepatic infla

38 ombinant IgG1 antibody to oxidized LDL (anti-oxLDL) in cynomolgus monkey.

39 were shown to induce the production of anti-oxLDL immunoglobulin M (IgM) antibodies, due to molecula

40 The clearance of anti-oxLDL is slightly higher than typical IgG1 antibodies in

41 The tissue biodistribution of anti-oxLDL was also investigated using positron emission tomo

42 used to measure serum concentrations of anti-oxLDL; Assay A was a ligand binding assay that measured

43 f 66 samples contained locally produced anti-oxLDL.

44 s, which were correlated with prominent anti-oxLDL immuno-staining (oxLDL-free regions: 497+/-55Omega

45 as associated with increased protective anti-oxLDL IgM.

46 Surprisingly, high-titer anti-oxLDL IgM production and reduced atherosclerosis was dep

47 bound forms) and Assay B measured total anti-oxLDL.

48 arry the same oxidation-specific epitopes as oxLDL.

49 om NO donors or pathological stimuli such as oxLDL triggers direct S-glutathiolation of p21ras Cys-11

50 In functional assays, oxLDL abolished guanosine 3',5'-cyclic monophosphate (cG

51 ress (ISS) provided a new strategy to assess oxLDL-laden lesions in the fat-fed New Zealand White (NZ

52 0B', which co-localized with cell-associated oxLDL-IC.

53 SP70B' co-localized with membrane-associated oxLDL-IC as well as the lipid moiety of internalized oxL

54 ion of low shear stress (SS) and atherogenic oxLDL.

55 vitro studies revealed that SS31 attenuated oxLDL-induced CD36 expression and foam cell formation in

56 s increased oxLDL accumulation and augmented oxLDL-mediated up-regulation of the C3 gene.

57 cytic vesicle fission, significantly blocked oxLDL uptake and inhibited foam cell formation.

58 We found that both oxLDL and oxidized linoleic acid derivatives indirectly

59 lateral nephrectomy and a high-fat diet, but oxLDL did not rise.

60 activation and mobilization of dynamin 2 by oxLDL was impaired in vav null cells.

61 Upregulation of miR-92a by oxLDL in atheroprone areas promotes endothelial activati

62 thway is required for platelet activation by oxLDL and may provide insights related to development of

63 Thus, we have identified LOX-1 activation by oxLDL and subsequent peroxynitrite generation as a novel

64 ily kinases abolished platelet activation by oxLDL in vitro.

65 92a regulated endothelial cell activation by oxLDL, more specifically under low SS conditions, which

66 uble E2 to SR-BI or CD81 was not affected by oxLDL, suggesting that oxLDL does not act as a simple re

67 ritical in promoting platelet aggregation by oxLDL.

68 iated with hypercholesterolemia is caused by oxLDL-mediated induction of TF expression in monocytes v

69 release, and caspase-3 activation induced by oxLDL in HUVECs.

70 The effects induced by oxLDL were inhibited by blocking LOX-1 scavenger recepto

71 i) macrophage foam cell formation induced by oxLDL, and (iii) platelet activation by oxPC(CD36).

72 ly kinases abolished Vav1 phosphorylation by oxLDL in vitro.

73 nase activity reduced JNK phosphorylation by oxLDL.

74 Taken together, JAM-C is up-regulated by oxLDL and may thereby contribute to increased inflammato

75 The synthesis of ROS by oxLDL/CD36 required Src-family kinases and protein kinas

76 mediating the induction of GSH synthesis by oxLDL and in protecting macrophages against oxidized lip

77 against endothelial dysfunction triggered by oxLDL.

78 t protein-transfected mouse RAW 264.7 cells, oxLDL-IC-induced HSP70B' co-localized with membrane-asso

79 Measurement of circulating oxLDL with antibody 4E6, has been widely used in many st

80 Our results suggest that circulating oxLDL, measured with antibody 4E6, is not an independent

81 independent of lipid markers and to compare oxLDL, apolipoprotein B100 (apoB), and total cholesterol

82 or of CHD independent of lipids and compared oxLDL with other important lipid predictors.

83 In conclusion, oxLDL induces BMP-2 expression through TLR2 and TLR4 in

84 role of this receptor cloned against copper-oxLDL, we examined whether it mediates EC uptake of L5,

85 LDL uptake, we used a fluorescent oxLDL (Dii-oxLDL) live cell assay with confocal microscopy imaging.

86 Dil-oxLDL and rMBSA taken up into MSC endosomes colocalized

87 p-regulation of Prx I expression with either oxLDL or ethoxyquin led to increased p38 MAPK activation

88 d, but in HCV-negative sera, high endogenous oxLDL had a negative effect on HCV infectivity in vitro.

89 mechanism of action, and whether endogenous oxLDL shares the anti-HCV properties of in vitro-generat

90 Finally, oxLDL IC-mediated IL-1beta production resulted in increa

91 Under arterial flow, oxLDL triggered sustained generation of platelet intrace

92 mediated oxLDL uptake, we used a fluorescent oxLDL (Dii-oxLDL) live cell assay with confocal microsco

93 onsistent with the importance of Lys-164 for oxLDL binding, SSO inhibited oxLDL uptake by macrophages

94 Here, we describe a mechanism for oxLDL-mediated platelet hyperactivity that requires gene

95 Nevertheless, cholesterol-free oxLDL and unmodified cholesterol (20 mug/ml) induce only

96 in HA accumulation because cholesterol-free oxLDL failed to induce HA synthesis.

97 -1beta compared with BMDCs treated with free oxLDL, whereas there was no difference in levels of TNF-

98 Oxidative stress resulting from oxLDLs and high glucose is additive.

99 Furthermore, oxLDL was co-localized with TLR2 and TLR4.

100 he anti-HCV properties of in vitro-generated oxLDL.

101 gical symptoms ensue, our findings highlight oxLDL, LOX-1, and peroxynitrite as important therapeutic

102 DL) and immune complexes prepared with human oxLDL and purified human antibodies to oxLDL (oxLDL-IC)

103 rambled peptides, effectively prevented: (i) oxLDL binding to CD36, (ii) macrophage foam cell formati

104 sors, we provided a new strategy to identify oxLDL-laden lesions.

105 -kappaB and MAPK pathways were comparable in oxLDL-loaded Mvarphis, yet the binding of p65/RelA (the

106 The involvement of nuclear factor kappaB in oxLDL uptake was validated in peritoneal macrophages in

107 our data show that activation of p38 MAPK in oxLDL-treated macrophages was dependent on the up-regula

108 These findings implicate Vav proteins in oxLDL-mediated platelet activation and suggest that Vav

109 (e.g., IL-1beta, IL-6, CCL5) was reduced in oxLDL-loaded cells at the level of transcription.

110 on withdrawing the HF diet, the reduction in oxLDL accumulation, as demonstrated with LO1-750, was le

111 The roles of TLR2 and TLR4 in oxLDL-induced BMP-2 expression were determined by pretre

112 es of Toll-like receptor (TLR) 2 and TLR4 in oxLDL-induced BMP-2 expression, and the signaling pathwa

113 scription and secretion as well as increased oxLDL accumulation and augmented oxLDL-mediated up-regul

114 exogenous FA in serum-free medium increased oxLDL binding and uptake to levels found with serum and

115 Mice on a high-fat diet have increased oxLDLs and systemic and nerve oxidative stress.

116 Vav1/Vav3 deficiency significantly inhibited oxLDL-mediated integrin alphaIIbbetaIII activation of pl

117 of Lys-164 for oxLDL binding, SSO inhibited oxLDL uptake by macrophages.

118 as well as the lipid moiety of internalized oxLDL-IC.

119 and dynamin 2 colocalized with internalized oxLDL in macrophages and that activation and mobilizatio

120 ly, in response to oxidatively modified LDL (oxLDL) and immune complexes prepared with human oxLDL an

121 emic mice and that oxidatively modified LDL (oxLDL) induces activation of macrophage Vav in vitro in

122 ndothelial cells (HUVECs) from oxidised LDL (oxLDL)-mediated dysfunction in vitro was investigated as

123 d higher plasma levels of both oxidized LDL (oxLDL) and cLDL compared with control mice.

124 a 260% increase of circulating oxidized LDL (oxLDL) binding to its receptor, LOX-1, and subsequent ge

125 is triggered by recognition of oxidized LDL (oxLDL) by Kupffer cells (KCs).

126 We previously showed that oxidized LDL (oxLDL) formed in the setting of hyperlipidemia and ather

127 ia leads to elevated levels of oxidized LDL (oxLDL) in plasma and that this induces expression of the

128 that CD36-dependent uptake of oxidized LDL (oxLDL) in vitro and foam cell formation in vitro and in

129 rkedly stimulate the uptake of oxidized LDL (oxLDL) into adipocytes, and this requires OLR1.

130 o found to internalize LDL and oxidized LDL (oxLDL) readily.

131 that the single-transmembrane oxidized LDL (oxLDL) receptor (LOX-1) resides in proximity to AT1 on c

132 Therefore, we measured oxidized LDL (oxLDL), advanced glycation end products-modified LDL (AG

133 igration assays, we found that oxidized LDL (oxLDL), but not native LDL, inhibited migration of WT mo

134 atelet function via binding to oxidized LDL (oxLDL), cell-derived microparticles, and thrombospondin-

135 the effect of rosiglitazone on oxidized LDL (oxLDL)-induced apoptosis.

136 experimentally prepared copper-oxidized LDL (oxLDL).

137 Oxidized low density lipoprotein (LDL; oxLDL) causes displacement of eNOS from caveolae by bind

138 neurons from adult rat using oxidized LDLs (oxLDLs).

139 In conclusion, the SR-BI ligand oxLDL is a potent cell entry inhibitor for a broad range

140 ia interaction with the receptor lectin-like oxLDL receptor (LOX)-1 and subsequent NAD(P)H oxidase ac

141 on between oxidized low-density lipoprotein (oxLDL) and CD36 inhibits macrophage migration; in the cu

142 (CD36) and oxidized low density lipoprotein (oxLDL) binding to CD36.

143 ly labeled oxidized low-density lipoprotein (oxLDL) by a monocyte/macrophage cell line.

144 native and oxidized low-density lipoprotein (oxLDL) by macrophages (Mvarphis) and foam cell formation

145 howed that oxidized low-density lipoprotein (oxLDL) formed in the setting of hyperlipidemia and ather

146 Oxidized low-density lipoprotein (oxLDL) has been reported as an inhibitor of hepatitis C

147 ereas anti-oxidized low-density lipoprotein (oxLDL) IgG likely promotes disease.

148 xposure to oxidized low-density lipoprotein (oxLDL) in vitro, we tested the hypothesis that oxLDL may

149 rotein and oxidized low density lipoprotein (oxLDL) increase C3 gene expression and protein secretion

150 irculating oxidized low-density lipoprotein (oxLDL) is a predictor of coronary heart disease (CHD) in

151 Oxidized low-density lipoprotein (oxLDL) is known to activate inflammatory responses in a

152 the plasma oxidized low-density lipoprotein (oxLDL) levels in mice and prevented oxLDL-mediated proli

153 effect of oxidized low density lipoprotein (oxLDL) on BMP-2 protein expression in human coronary art

154 lipids in oxidized low-density lipoprotein (oxLDL) particles, a process that induces an overt prothr

155 Oxidized low-density lipoprotein (oxLDL) promotes unregulated platelet activation in dysli

156 ophages to oxidized low density lipoprotein (oxLDL) triggers the differential expression of a number

157 on FA and oxidized low density lipoprotein (oxLDL) uptake.

158 Oxidized low-density lipoprotein (oxLDL), but not native LDL, potently inhibited HCVpp and

159 Retained oxidized low-density lipoprotein (oxLDL), in turn, stimulated myofibroblastic VIC differen

160 model for oxidised low density lipoprotein (oxLDL)-induced lipid accumulation in macrophages.

161 on between oxidized low-density lipoprotein (oxLDL)-induced prothrombotic platelet signaling and the

162 esponse to oxidized low density lipoprotein (oxLDL)-laden lesions.

163 including oxidized low-density lipoprotein (oxLDL).

164 ns such as oxidized low-density lipoprotein (oxLDL).

165 ed against oxidized low-density lipoprotein (oxLDL).

166 In the oxidized low-density-lipoprotein (oxLDL)-rich lesions from explants of fat-fed rabbits, im

167 ic lipids (oxidized low density lipoprotein [oxLDL] and oxidized linoleic acid derivatives) induce ad

168 lation of oxidized low-density lipoproteins (oxLDL) and increasing inflammatory responses.

169 Oxidized low density lipoproteins (oxLDL) are among the ligands that bind to CD36 and are e

170 uptake of oxidized low-density lipoproteins (oxLDL) by macrophages leading to conversion into foam ce

171 uptake of oxidized low density lipoproteins (oxLDL) by macrophages.

172 Oxidized low-density lipoproteins (oxLDL) generated in the hyperlipidemic state may contrib

173 donor or oxidized low-density lipoproteins (oxLDL) increases p21ras activity in bovine aortic endoth

174 s against modified low-density lipoproteins (oxLDL), leading to plaque reduction.

175 ated with oxidized low-density lipoproteins (oxLDL).

176 HCV particles entering target cells lost oxLDL sensitivity with time kinetics parallel to anti-SR

177 l cholesterol (P < 0.00003) levels yet lower oxLDL/LDL (P = 0.006) and sPLA2-IIA mass (P = 0.04), pro

178 ole that each FA might play in CD36-mediated oxLDL uptake, we used a fluorescent oxLDL (Dii-oxLDL) li

179 rat astrocytes, and that exposure to minimal oxLDL stimulated astrocyte interleukin-6 secretion but d

180 We further demonstrated that minimally oxLDL was most effectively internalized by primary cultu

181 enotypes, with genotype 4 appearing the most oxLDL sensitive.

182 Although the ability of oxLDL to activate platelets is established, the underlyi

183 , we assessed whether i.v. administration of oxLDL-induced apoptotic DCs (apop(ox)-DCs) and, as a con

184 ients was characterized by the appearance of oxLDL epitopes in astrocytes, but not neurons or microgl

185 n cell-surface membranes and that binding of oxLDL to LOX-1 can allosterically activate AT1-dependent

186 an enhanced capacity to block the binding of oxLDL to macrophages.

187 and Gclm promoters resulted in a decrease of oxLDL-induced luciferase activity.

188 d activation of Rac, abrogated the effect of oxLDL.

189 f HCVpp, suggesting a ternary interaction of oxLDL with both virus and target cells.

190 lucidate the link between internalization of oxLDL and HA production in vitro, using human aortic smo

191 rom PfnHet showed blunted internalization of oxLDL and oxLDL-induced inflammation.

192 Levels of oxLDL ICs often correlate with disease severity, and stu

193 The levels of oxLDL were also significantly improved with the consumpt

194 Levels of oxLDL, AGE-LDL, and MDA-LDL were measured in circulating

195 by the relative electrophoretic mobility of oxLDL, the fragmentation of ApoB, conjugated diene produ

196 -associated and internalized lipid moiety of oxLDL-IC.

197 (+) T cells that expanded in the presence of oxLDL induced more profound experimental autoimmune ence

198 Macrophage migration in the presence of oxLDL was restored by both antioxidants and NADPH oxidas

199 als in the highest versus lowest quartile of oxLDL and AGE-LDL in IC had a 6.11-fold [confidence inte

200 rotein content, which is within the range of oxLDL reported to be present in human plasma.

201 To inhibit recognition of oxLDL by KCs, low-density lipoprotein receptor (Ldlr(-/-

202 CD36-dependent uptake of oxLDL in vitro and foam cell formation in vitro and in v

203 Moreover, the uptake of oxLDL induced dendritic-cell-mediated Th17 cell polariza

204 Antibody-mediated uptake of oxLDL or bacteria dramatically enhances DC-IL-12, and DC

205 Binding/uptake of oxLDL was dependent upon the FA dose, except for docosah

206 g to CD36 but did not activate the uptake of oxLDL.

207 Dyslipidemia leads to high levels of oxLDLs that may injure DRG neurons via LOX-1 and contrib

208 The underlying mechanism was dependent on oxLDL-mediated CD36 signaling, which resulted in sustain

209 inding to CD36 and the effects of each FA on oxLDL uptake have important implications for protein con

210 l undergoes modifications such as oxidation (oxLDL).

211 xLDL and purified human antibodies to oxLDL (oxLDL-IC) in monocytic and macrophage cell lines.

212 t KFEE may protect LDL oxidation and prevent oxLDL-induced cellular dysfunction in HUVECs.

213 protein (oxLDL) levels in mice and prevented oxLDL-mediated proliferative response in human breast ad

214 letion of ERK5 in murine platelets prevented oxLDL-induced platelet deposition on immobilized collage

215 ypercholesterolemic mice and monkeys reduced oxLDL, monocyte TF expression, MP TF activity, activatio

216 or silencing of these two receptors reduced oxLDL-induced BMP-2 expression.

217 ay, demonstrating that Vav proteins regulate oxLDL uptake and foam cell formation via calcium- and dy

218 Serum oxLDL levels are decreased in both lean and obese diabet

219 y HCV-infected individuals, endogenous serum oxLDL levels did not correlate with viral load, but in H

220 After 9 weeks of HD, serum oxLDL levels (mg/dL) increased by 140 fold, accompanied

221 d with prominent anti-oxLDL immuno-staining (oxLDL-free regions: 497+/-55Omega, n=8 vs. oxLDL-rich le

222 gh a separate and more robust mechanism than oxLDL alone and that these ICs may be immunomodulatory i

223 cells of cerebrum after infarction and that oxLDL may influence the pathophysiology of cerebral infa

224 Collectively, these data demonstrate that oxLDL ICs induce inflammasome activation through a separ

225 ease severity, and studies demonstrated that oxLDL ICs elicit potent inflammatory responses in macrop

226 focal microscopy, however, demonstrated that oxLDL-IC stimulated the release of HSP70B', which co-loc

227 This study demonstrates that oxLDL and hyperlipidemia stimulate the generation of NOX

228 We found that oxLDL inhibits HCVcc at least as potently as HCV pseudop

229 port of this hypothesis, we report here that oxLDL induced TF expression in human monocytic cells and

230 LDL) in vitro, we tested the hypothesis that oxLDL may be present in parenchymal cells of cerebrum af

231 current study we tested the hypothesis that oxLDL/CD36-induced inhibition of migration is the result

232 activation of RhoA and ROCK, indicating that oxLDL regulates contractile signaling through a tyrosine

233 This study revealed that oxLDL loading of Mvarphis negatively regulates transcrip

234 We show that oxLDL stimulate platelet activation through phosphorylat

235 Live cell imaging of macrophages showed that oxLDL actuated retraction of macrophage front end lamell

236 Chimeric analysis showed that oxLDL-induced AT1 signaling events are mediated via inte

237 In conclusion, these findings suggest that oxLDL-IC induce the synthesis and release of HSP70B', an

238 ntly earlier than anti-CD81, suggesting that oxLDL acts by perturbing interaction between HCV and SR-

239 1 was not affected by oxLDL, suggesting that oxLDL does not act as a simple receptor blocker.

240 results demonstrate for the first time that oxLDL is present in brain parenchyma of patients with is

241 The oxLDL was measured via enzyme-linked immunosorbent assay

242 the possible damage of vessels caused by the oxLDL.

243 vesicles had a high binding affinity for the oxLDL binding site of the CD36 receptor and participated

244 concentrations similar to those found in the oxLDL also indicated that 7kCh is the most cytotoxic of

245 d receptor agonist was found to increase the oxLDL uptake of macrophages.

246 Interestingly, much of the oxLDL in circulation is complexed to Abs, and these resu

247 Analysis of the oxLDL showed a predominance of the 7-oxygenated products

248 t mechanism to enhance the metabolism of the oxLDL that could prevent both lipid accumulation and foa

249 Consistent with this, oxLDL induced tyrosine phosphorylation of a number of pr

250 zed sterol-related species delivered through oxLDL.

251 At the same time, oxLDL incubation altered the biophysical properties of H

252 human oxLDL and purified human antibodies to oxLDL (oxLDL-IC) in monocytic and macrophage cell lines.

253 Antibodies to oxLDL play an important role in the pathogenesis of NASH

254 in kinase pathway importantly contributes to oxLDL-mediated induction of MMP2 expression.

255 This inflammasome priming was due to oxLDL IC signaling via multiple receptors, because inhib

256 receptor (LXR) in the macrophages exposed to oxLDL.

257 d9 null and cd36 null macrophages exposed to oxLDL.

258 associated with Vav1 in platelets exposed to oxLDL.

259 osine phosphorylated in platelets exposed to oxLDL.

260 were phosphorylated in platelets exposed to oxLDL.

261 re recruited to CD36 in platelets exposed to oxLDL.

262 ical mechanism leading from hyperglycemia to oxLDL formation and eNOS dysfunction is unknown.

263 pheral blood monocyte-derived macrophages to oxLDL.

264 this would determine platelet reactivity to oxLDL.

265 therefore that CD36 signaling in response to oxLDL alters cytoskeletal dynamics to enhance macrophage

266 et activation and aggregation in response to oxLDL and targeted genetic deletion of ERK5 in murine pl

267 ation of Prx I in macrophages in response to oxLDL exposure and its ability to function as both antio

268 decreased IL-1beta secretion in response to oxLDL ICs.

269 decreased IL-1beta secretion in response to oxLDL ICs.

270 and TLR4 in mediating the BMP-2 response to oxLDL in human CAECs and indicate that these two immunor

271 TLR4 enhanced the cellular BMP-2 response to oxLDL.

272 87) between platelet activation responses to oxLDL and level of CD36 expression.

273 ely, correlates with functional responses to oxLDL, and is associated with inheritance of specific CD

274 nd leukocyte transendothelial migration upon oxLDL treatment of endothelial cells, whereas JAM-C on q

275 Thus, upon oxLDL stimulation endothelial JAM-C functions as both an

276 In vitro, oxLDLs lead to severe DRG neuron oxidative stress via in

277 (oxLDL-free regions: 497+/-55Omega, n=8 vs. oxLDL-rich lesions: 679+/-125Omega, n=12, P<0.05).

278 When oxLDL and apoB were mutually adjusted, only apoB was pre

279 Similar results were found when oxLDL and TC/HDL-C ratio were mutually adjusted.

280 However, when oxLDL, LDL cholesterol, HDL-C, and triglycerides were mu

281 nd protein secretion in macrophages, whereas oxLDL differently modulates LPS-mediated regulation of C

282 tivation and suggest a new mechanism whereby oxLDL may be promoting risk for cardiovascular disease.

283 n and suggest a potential mechanism by which oxLDL may activate innate immunity and thereby indirectl

284 The results support a model in which oxLDL uptake is dependent on the activation of multiple

285 for most of the cytotoxicity associated with oxLDL internalization in ARPE19 cells.

286 Treatment of BMDCs with oxLDL ICs increased expression of inflammasome-related g

287 DL-R with the internalized LDL and CD36 with oxLDL particles.

288 rived dendritic cells (BMDCs) incubated with oxLDL ICs for 24 h secrete significantly more IL-1beta c

289 IFN-beta was inhibited in cells loaded with oxLDL, whereas the induction of other proinflammatory ge

290 Loading with oxLDL did not induce peritoneal Mvarphi apoptosis or mod

291 cells and mouse peritoneal macrophages with oxLDL.

292 M) antibodies, due to molecular mimicry with oxLDL.

293 ients with elevated antibodies reactive with oxLDL could be a subgroup at high risk for cardiovascula

294 Human CAECs were stimulated with oxLDL.

295 Stimulation with oxLDL increased cellular BMP-2 protein levels in a dose-

296 We combined molecular virology tools with oxLDL serum measurements in different patient cohorts to

297 ditioned medium from U937 cells treated with oxLDL alone revealed an increase in intracellular HSP70B

298 reased foam cell formation when treated with oxLDL, attributable in part to increased expression of s

299 roved cell survival following treatment with oxLDL or tert-butyl hydroperoxide.

300 Among both men and women, oxLDL was significantly related to risk of CHD in multiv