ライフサイエンスコーパス: aortic endothelial cell

1 higher in microvascular endothelium than in aortic endothelial cells.

2 ulation and biopterin metabolism in cultured aortic endothelial cells.

3 A-knockout mice or primary cultures of their aortic endothelial cells.

4 ROS levels induced by palmitic acid in human aortic endothelial cells.

5 tion of von Willebrand factor in MSU-treated aortic endothelial cells.

6 the association of AMPK with LKB1 in bovine aortic endothelial cells.

7 d the effects of metformin on AMPK in bovine aortic endothelial cells.

8 eciprocally decrease endothelial NO in human aortic endothelial cells.

9 isolated PGHS and prostacyclin formation by aortic endothelial cells.

10 O production and hsp90 association in bovine aortic endothelial cells.

11 d for translocation of Hsp90alpha in porcine aortic endothelial cells.

12 OS in cell lysates from proliferating bovine aortic endothelial cells.

13 ranslocation of Hsp90alpha to the outside of aortic endothelial cells.

14 ivin-like kinase receptor 1 (ALK1) in bovine aortic endothelial cells.

15 y of a target protein (caspase-3), in bovine aortic endothelial cells.

16 p to 70- and 15-fold, respectively, in human aortic endothelial cells.

17 ion of S1P1, S1P2, and S1P3 receptors on NOD aortic endothelial cells.

18 (oxLDL) increases p21ras activity in bovine aortic endothelial cells.

19 echanism of the rPAI-1(23) effects in bovine aortic endothelial cells.

20 K293 cells and increased apoptosis in bovine aortic endothelial cells.

21 lated by E2F1 upon VEGF stimulation of human aortic endothelial cells.

22 h-induced stress fiber orientation in bovine aortic endothelial cells.

23 o effect on the elastic properties of bovine aortic endothelial cells.

24 and oxysterols elevated profilin in cultured aortic endothelial cells.

25 lesterol on membrane deformability of bovine aortic endothelial cells.

26 dation, and apoptosis in H2O2-treated bovine aortic endothelial cells.

27 were examined during wound healing by bovine aortic endothelial cells.

28 e increase interleukin-8 (IL-8) synthesis in aortic endothelial cells.

29 nduced by IFN-gamma (Mig) in a pool of human aortic endothelial cells.

30 ntly associated with reduced PPAP2B in human aortic endothelial cells.

31 athways that regulate NO production in human aortic endothelial cells.

32 lower oxidative stress was tested in bovine aortic endothelial cells.

33 stress in response to hyperglycemia in human aortic endothelial cells.

34 2)O(2)-induced permeability change in bovine aortic endothelial cells.

35 expression of inflammatory genes in porcine aortic endothelial cells.

36 increases cytosolic Ca(2+) concentration in aortic endothelial cells.

37 2 degrees C for 2 h, hyperthermia) in bovine aortic endothelial cells.

38 In aortic endothelial cells, 7-ketocholesterol enhanced STA

39 Gb3 in cultured alpha-Gal A-deficient mouse aortic endothelial cells accumulated in endothelial plas

40 By 4 mo of age, alpha-Gal A -/0 mouse aortic endothelial cells achieved their peak Gb3 levels.

41 e one against a comparable somatic cell, the aortic endothelial cell (AEC).

42 Migration and proliferation of aortic endothelial cells (AEC) are critical processes in

43 l microvascular endothelial cells (RMEC) and aortic endothelial cells (AEC) from a GGTA1/CMAH double-

44 product of HE and O(2)(.-) formed in bovine aortic endothelial cells after treatment with menadione

45 individual components and mixtures in bovine aortic endothelial cells and A549 cells.

46 53 in DOX-induced apoptosis in normal bovine aortic endothelial cells and adult rat cardiomyocytes an

47 We added ceramide to human aortic endothelial cells and assayed Weibel-Palade body

48 CDK5, P25, accumulated in senescent porcine aortic endothelial cells and atherosclerotic aortas.

49 on LPS plus S1P treatment of HUVEC and human aortic endothelial cells and cell-type differences on p3

50 We then stimulated primary aortic endothelial cells and ex-vivo atherosclerotic tis

51 ingivalis are required for invasion of human aortic endothelial cells and for the stimulation of pote

52 olayer, we disrupted FGF signaling in bovine aortic endothelial cells and human saphenous vein endoth

53 Both bovine aortic endothelial cells and human umbilical endothelial

54 Therefore, primary mouse aortic endothelial cells and human umbilical vein endoth

55 the presence of protein S and Gas6 in human aortic endothelial cells and human umbilical vein endoth

56 Gab1 tyrosine phosphorylation in both bovine aortic endothelial cells and human umbilical vein endoth

57 f Arg2 from mitochondria to cytosol in human aortic endothelial cells and in murine aortic intima wit

58 ion of the profibrotic cytokine TGF-beta1 in aortic endothelial cells and Ly6C(low) macrophages.

59 ted with reduced ADAMTS7 expression in human aortic endothelial cells and lymphoblastoid cell lines.

60 class 1-like molecule expressed in lesional aortic endothelial cells and macrophage-rich regions, as

61 rly events of atherosclerosis using cultured aortic endothelial cells and monocytes as a vascular mod

62 Porcine aortic endothelial cells and murine Balb/3T3 cells were

63 eaction revealed the expression of nmMLCK in aortic endothelial cells and peripheral blood monocytes.

64 s tonically S-nitrosylated in resting bovine aortic endothelial cells and that the enzyme undergoes r

65 ER export of DAT was demonstrated in porcine aortic endothelial cells and the immortalized neuronal c

66 tor demonstrated a lack of toxicity in human aortic endothelial cells and zebrafish.

67 e in human umbilical vein endothelial cells, aortic endothelial cells, and endothelium-derived cell l

68 inhibited LNO(2) induction of HO-1 in human aortic endothelial cells, and LNO(2) activated a 4.5-kb

69 cell adhesion molecule-1 expression in human aortic endothelial cells, and reduced cholesterol efflux

70 own a series of signaling proteins in bovine aortic endothelial cells, and we have combined biochemic

71 We recently reported that in aortic endothelial cells, Ang II induces endothelial nit

72 rly events of atherosclerosis using cultured aortic endothelial cells as a vascular model system, for

73 suppressed VEGF expression, respectively, in aortic endothelial cells, as determined by real-time pol

74 eated HAECs increased angiogenesis in bovine aortic endothelial cells, as mediated by BMP-4, and oste

75 ivity of >700-fold and was nontoxic to human aortic endothelial cells at 100 muM.

76 In human aortic endothelial cells, BA increased beta1-integrin-Ar

77 In bovine or human aortic endothelial cells (BAEC and HAEC), treatment with

78 We now report that LPA treatment of bovine aortic endothelial cells (BAEC) activates eNOS enzyme ac

79 nd that insulin treatment of cultured bovine aortic endothelial cells (BAEC) activates the alpha isof

80 ed in S1P-mediated Rac1 activation in bovine aortic endothelial cells (BAEC) and found that S1P-induc

81 found that CaM is a phosphoprotein in bovine aortic endothelial cells (BAEC) and that the kinase CK2

82 We used intraluminal bovine aortic endothelial cells (BAEC) co-cultured with extralu

83 ced oxidative stress and apoptosis in bovine aortic endothelial cells (BAEC) through enhanced scaveng

84 on NO*-mediated apoptosis, we exposed bovine aortic endothelial cells (BAEC) to (Z)-1-[N-(2-aminoethy

85 Exposure of bovine aortic endothelial cells (BAEC) to chemically synthesize

86 ing the adhesion and proliferation of bovine aortic endothelial cells (BAEC) using a ZnO nanostructur

87 To test this hypothesis, bovine aortic endothelial cells (BAEC) were subjected to LS (15

88 Treatment of bovine aortic endothelial cells (BAEC) with EGCG (50 microm) ac

89 ed signaling pathways, we transfected bovine aortic endothelial cells (BAEC) with small interfering R

90 duction in a dose-dependent manner in bovine aortic endothelial cells (BAEC), and this was inhibited

91 y increases eNOS activity in cultured bovine aortic endothelial cells (BAEC).

92 t targeted specific VEGFR subtypes in bovine aortic endothelial cells (BAEC).

93 LC3-II and autophagosomes in primary bovine aortic endothelial cells (BAEC).

94 In both bovine aortic endothelial cells (BAECs) and NIH3T3 cells expres

95 ynitrite was investigated in cultured bovine aortic endothelial cells (BAECs) by measuring superoxide

96 studies demonstrated that MNP-loaded bovine aortic endothelial cells (BAECs) could be magnetically t

97 Bovine aortic endothelial cells (BAECs) exposed to black tea po

98 K activity were monitored in cultured bovine aortic endothelial cells (BAECs) exposed to HOG-LDL or i

99 e tyrosine phosphorylation of eNOS in bovine aortic endothelial cells (BAECs) exposed to oxidant stre

100 Bovine aortic endothelial cells (BAECs) in the presence of 50 m

101 pitation and affinity purification in bovine aortic endothelial cells (BAECs) that Cdc37 is complexed

102 e-mediated phosphorylation of eNOS in bovine aortic endothelial cells (BAECs) that is phosphorylated

103 Exposure of cultured bovine aortic endothelial cells (BAECs) to clinically relevant

104 Exposure of cultured bovine aortic endothelial cells (BAECs) to palmitate (0.4 mM) b

105 Bovine aortic endothelial cells (bAECs) were incubated in serum

106 esults in an increase of apoptosis in bovine aortic endothelial cells (BAECs), as determined by termi

107 In bovine aortic endothelial cells (BAECs), the effects of vascula

108 ritical activator of AMPK in cultured bovine aortic endothelial cells (BAECs).

109 y in eNOS-transfected COS-7 cells and bovine aortic endothelial cells (BAECs).

110 h eNOS 3'-UTR in both COS-7 cells and bovine aortic endothelial cells (BAECs).

111 , tube formation and cell invasion in bovine aortic endothelial cells (BAECs).

112 els are associated with caveolin-1 in bovine aortic endothelial cells (BAECs).

113 s in C(2)-ceramide (C(2)-cer)-treated bovine aortic endothelial cells (BAECs).

114 ter reporter construct in transfected bovine aortic endothelial cells (BAECs).

115 o determine [Ca(2+)] in Fluo-3-loaded bovine aortic endothelial cells (BAECs).

116 eNOS was determined in rat aortas and bovine aortic endothelial cells (BAECs).

117 lycemic conditions, sirolimus impaired human aortic endothelial cell barrier function, migration, and

118 or pathways of hyperglycemic damage found in aortic endothelial cells by inhibiting GAPDH activity.

119 The addition of H(2)O(2) to bovine aortic endothelial cells caused a potent and dose-depend

120 erol in cultured alpha-Gal A-deficient mouse aortic endothelial cell caveolae.

121 man monocytic leukemia THP-1 cells and human aortic endothelial cells compared with zinc-deficient ce

122 demonstrate that isolated pulmonary (but not aortic) endothelial cells constrict in hypoxia.

123 Bovine aortic endothelial cells cultured in compliant or stiff

124 Bovine aortic endothelial cell cultures exposed to a 500-microM

125 ified low-density lipoprotein was reduced in aortic endothelial cells derived from MyD88-deficient mi

126 (25 mm) increases monocyte adhesion to human aortic endothelial cells (EC).

127 ration of IL8RA- and/or IL8RB-transduced rat aortic endothelial cells (ECs) accelerates adhesion of E

128 We isolated aortic endothelial cells (ECs) from B6 and G2A(-/-) mice

129 Using isolated primary aortic endothelial cells (ECs) from db/db mice and WEHI7

130 hematopoietic stem cells (HSCs) emerge from aortic endothelial cells (ECs) through an intermediate s

131 AhR was expressed in aortic endothelial cells (ECs), activated, and bound to

132 titive passages, primary cultures of porcine aortic endothelial cells exhibited a severe senescence p

133 Porcine aortic endothelial cells exhibited time- and concentrati

134 In cultured human aortic endothelial cells exposed to 30 mmol/L glucose, w

135 F2 expression was decreased in primary human aortic endothelial cells exposed to bacterial lipopolysa

136 Experiments in human aortic endothelial cells exposed to high glucose were pe

137 Human aortic endothelial cells exposed to hyperglycemic condit

138 ce vascular cell adhesion molecule levels on aortic endothelial cells exposed to MPO-oxidized HDL.

139 pression was reduced in the human- and mouse aortic endothelial cells exposed to oscillatory shear in

140 rapid increase in arginase activity in human aortic endothelial cells exposed to oxidized low-density

141 Sck is not observed in VEGF-treated porcine aortic endothelial cells expressing a receptor mutated a

142 s and in high glucose-treated primary murine aortic endothelial cells expressing hAR.

143 LR2 or TLR4 reduced IL-8 production by human aortic endothelial cells following stimulation with majo

144 Treating bovine aortic endothelial cells for 24 h with 30 mug/ml cholest

145 , as determined by comparing the currents in aortic endothelial cells freshly isolated from healthy o

146 n umbilical vein endothelial cells and mouse aortic endothelial cells from AMPK-deficient mice were u

147 In addition, mouse aortic endothelial cells from AMPKalpha2 knockout (AMPKa

148 Analysis of aortic endothelial cells from AMPKalpha2(-/-) mice and h

149 edly reduced the level of ER stress in mouse aortic endothelial cells from AMPKalpha2(-/-) mice.

150 y with increased oxidation of SERCA in mouse aortic endothelial cells from AMPKalpha2(-/-) mice.

151 l boundary from E7.5 and weakly in embryonic aortic endothelial cells from E13.5, suggesting that ext

152 In summary, primary cultures of aortic endothelial cells from Fabry mice retain the phen

153 itions for the growth of primary cultures of aortic endothelial cells from wild-type and alpha-Gal A

154 In bovine aortic endothelial cells, GAPDH antisense oligonucleotid

155 )496-507 was examined for induction of human aortic endothelial cell (HAEC) activation.

156 lerosis, we examined TLR expression in human aortic endothelial cells (HAEC) cultured with wild-type

157 nted in endothelial cells, we examined human aortic endothelial cells (HAEC) for CRP production.

158 at effective concentrations; protects human aortic endothelial cells (HAEC) from cold hypoxia/reoxyg

159 lysis of miR-10a knockdown in cultured human aortic endothelial cells (HAEC) identified IkappaB/NF-ka

160 ute regulation of VCAM-1 expression in human aortic endothelial cells (HAEC) in response to triglycer

161 tenance of [Ca(2+)](i) oscillations in human aortic endothelial cells (HAEC) stimulated by histamine.

162 ncy was evaluated in vitro by allowing human aortic endothelial cells (HAEC) to migrate onto microgro

163 Primary human aortic endothelial cells (HAEC) were stimulated with HLA

164 VCAM-1 mRNA and protein expression in human aortic endothelial cells (HAEC), has a relatively modest

165 In human aortic endothelial cells (HAEC), pretreatment with H89 (

166 18, a hallmark of c-src activation, in human aortic endothelial cells (HAEC).

167 mRNA levels without affecting TSP1 in human aortic endothelial cells (HAEC).

168 effect of 5,6-epoxyisoprostane, EI, on human aortic endothelial cells (HAEC).

169 d for its capacity to bind to cultured human aortic endothelial cells (HAECs) and alter the acute inf

170 of VEGF-A-responsive genes in primary human aortic endothelial cells (HAECs) and human umbilical vei

171 hat nesprin-3 is robustly expressed in human aortic endothelial cells (HAECs) and localizes to the nu

172 glucose-induced NF-kappaB activity in human aortic endothelial cells (HAECs) and subsequently suppre

173 x-LDL) induces the release of CRP from human aortic endothelial cells (HAECs) and to optimize several

174 cal vein endothelial cells (HUVECs) or human aortic endothelial cells (HAECs) derived from vessel wal

175 In human aortic endothelial cells (HAECs) exposed to high glucose

176 y, we determined the amine response of human aortic endothelial cells (HAECs) from a glucose challeng

177 own under hyperglycaemic conditions in human aortic endothelial cells (HAECs) hypothesizing that the

178 glucose increases monocyte adhesion to human aortic endothelial cells (HAECs) in vitro.1 In the prese

179 8, S100A12, and HMGB1 was evaluated in human aortic endothelial cells (HAECs) incubated in normal glu

180 ntitative polymerase chain reaction in human aortic endothelial cells (HAECs) revealed that sirolimus

181 aspase-1 activation in larger sizes of human aortic endothelial cells (HAECs) than in smaller sizes o

182 We subjected human aortic endothelial cells (HAECs) to hyperglycemic condit

183 mouse aorta and calpain activation in human aortic endothelial cells (HAECs) treated with DL-Hcy (50

184 nt of regulatory landscapes of primary human aortic endothelial cells (HAECs) under basal and activat

185 Human aortic endothelial cells (HAECs) were cultured within th

186 Human aortic endothelial cells (HAECs) were exposed to varying

187 Infection of primary human aortic endothelial cells (HAECs) with Ad-Nnat increased

188 nofluorescence, TNF-alpha treatment of human aortic endothelial cells (HAECs) with the control vector

189 Treatment of human aortic endothelial cells (HAECs) with the NF-kappaB inhi

190 induced a typical cytopathic effect in human aortic endothelial cells (HAECs), ie, the formation of s

191 mRNA and protein expression in primary human aortic endothelial cells (HAECs).

192 tokine signal transduction pathways in human aortic endothelial cells (HAECs).

193 synthase expression and bioactivity in human aortic endothelial cells (HAECs).

194 xamining the effect of CRP on PAI-1 in human aortic endothelial cells (HAECs).

195 vascular endothelial growth factor in human aortic endothelial cells (HAECs).

196 arterial endothelial cells in vivo and human aortic endothelial cells (HAoECs) in vitro.

197 re capable of recognizing xenogeneic porcine aortic endothelial cells in a calcium-dependent manner.

198 mbilical vein endothelial cells and in human aortic endothelial cells in a manner that is dependent o

199 In human aortic endothelial cells in culture, S18886 also prevent

200 Bovine aortic endothelial cells in primary culture loaded with

201 Moreover, matrix Gla protein-depleted human aortic endothelial cells in vitro acquire multipotency r

202 e growth of prostate cancer cells and bovine aortic endothelial cells in vitro, with a more potent ef

203 Analysis of primary aortic endothelial cells indicated that atheroprotective

204 Our initial experiments in bovine aortic endothelial cells indicated that exogenous NO dec

205 ls expressing wild type (WT) Panx1 and mouse aortic endothelial cells induced Panx1 S-nitrosylation.

206 ates and cGMP accumulation in intact porcine aortic endothelial cells infected with wild-type or muta

207 In bovine aortic endothelial cells, interaction between endogenous

208 verexpression of HD3alpha reprogrammed human aortic endothelial cells into mesenchymal cells featurin

209 hancer in transgenic embryos and in cultured aortic endothelial cells is dependent on four ETS sites.

210 olar lipid content of primary cultured mouse aortic endothelial cells isolated from alpha-Gal A null

211 potentiated HG-induced calpain activation in aortic endothelial cells isolated from Cbs mice.

212 Experiments in primary aortic endothelial cells isolated from mice and in cultu

213 e human breast cancer cell line), PAE (a pig aortic endothelial cell line) and HaCaT (the human kerat

214 In this study, using mouse aortic endothelial cells (MAEC) deficient in ICAM-1, we

215 In contrast to macrophages, murine aortic endothelial cells (MAEC) produced no NO in respon

216 d levels of Kindlin-2 in Kindlin-2(+/-) mice aortic endothelial cells (MAECs) from these mice, and hu

217 In cultured bovine aortic endothelial cells, metformin dose-dependently act

218 In conclusion, ROS production in bovine aortic endothelial cell mitochondria results largely fro

219 We used aortic endothelial cells obtained from C57BL/6 (MAE-C57)

220 in low concentrations in the human pulmonary aortic endothelial cells offered protection against depl

221 s of hCD152-hCD59 transduced primary porcine aortic endothelial cells or hCD152-hCD59 and pCD152-hCD5

222 In human aortic endothelial cells, OxLDL stimulation increased ar

223 ons in neovascularization in vivo in porcine aortic endothelial cell (PAEC)-VEGF/basic fibroblast gro

224 promote the recruitment of huTreg to porcine aortic endothelial cells (PAEC) and their capacity to re

225 nvestigate HMGB1-mediated effects on porcine aortic endothelial cells (PAEC) from wild-type (WT) and

226 d genetically modified (GTKO.hCD46.hTBM) pig aortic endothelial cells (PAEC) in two pig-to-human in v

227 ted antibodies were used to activate porcine aortic endothelial cells (PAEC) in vitro.

228 TF) in a functional assay in primary porcine aortic endothelial cells (PAEC) in vitro.

229 uman CD8+ CTL were generated against porcine aortic endothelial cells (PAEC).

230 e knockout (GalTKO)/hCD46-transgenic porcine aortic endothelial cells (PAEC).

231 osyltransferase gene-knockout (GTKO) porcine aortic endothelial cells (pAECs) was investigated.

232 is study, we showed that 16k PRL reduced rat aortic endothelial cell (RAEC) migration in a wound-heal

233 ed with HS6B-XO, the binding of XO to bovine aortic endothelial cells rendered the enzyme resistant t

234 Cultured aortic endothelial cells responded to myostatin with a r

235 id bilayers, cholesterol depletion of bovine aortic endothelial cells resulted in a significant decre

236 lls isolated from mice and in cultured human aortic endothelial cells revealed the central role of JN

237 ue of Cell, Matsushita et al. report that in aortic endothelial cells, S-nitrosylation of NSF, an ATP

238 Functional analysis in human aortic endothelial cells showed that the carriers of the

239 In human aortic endothelial cells, silencing of Set7 prevented mo

240 interfering RNA by as much as 86% in porcine aortic endothelial cells stably expressing human (h)DATs

241 ance (Gamma) in confluent cultures of bovine aortic endothelial cells subjected to continuous laminar

242 pha-mediated downregulation of eNOS in human aortic endothelial cells than did untreated MACs from pa

243 We found in bovine aortic endothelial cells that inhibitions of Rho, Rho-ki

244 In primary murine and human aortic endothelial cells, the PKCbeta-JNK mitogen-activa

245 Exposure of cultured bovine aortic endothelial cells to 1 mum CsA for 1 h significan

246 Specifically, exposing human aortic endothelial cells to acetylated low-density lipop

247 Exposure of cultured human aortic endothelial cells to clinically relevant concentr

248 We exposed porcine aortic endothelial cells to components of black tea and

249 cal vein endothelial cells (HUVECs) or mouse aortic endothelial cells to either IBOP or U46619, two s

250 med that PCC are more resistant than porcine aortic endothelial cells to human NK cell-mediated lysis

251 n umbilical vein endothelial cells or bovine aortic endothelial cells to metformin significantly incr

252 Exposure of mature aortic endothelial cells to netrin-1 resulted in a poten

253 Exposure of bovine aortic endothelial cells to ONOO- significantly increase

254 ediating the inflammatory responses of human aortic endothelial cells to oxidized phospholipids, we p

255 Exposure of confluent bovine aortic endothelial cells to simvastatin (statin) dose-de

256 Exposure of bovine aortic endothelial cells to simvastatin for 24 h strikin

257 HSS (65 dyn/cm(2)) was applied on bovine aortic endothelial cells to visualize the dynamic Src ac

258 toprotection of nitric oxide (*NO) in bovine aortic endothelial cells treated with H2O2.

259 thase (eNOS) expression was studied in human aortic endothelial cells treated with tumour necrosis fa

260 Furthermore, overexpressing profilin in rat aortic endothelial cells triggered 3 indicators of endot

261 ulture, reduced PPAP2B was measured in human aortic endothelial cells under atherosusceptible wavefor

262 FoxO4 knockdown in human aortic endothelial cells upregulated nitric oxide on isc

263 esis, we decreased G6PD expression in bovine aortic endothelial cells using an antisense oligodeoxynu

264 d in isolated mitochondria and intact bovine aortic endothelial cells using electron spin resonance,

265 were further confirmed in vivo in a porcine aortic endothelial cell-vascular endothelial growth fact

266 es could not be identified in the canine VWD aortic endothelial cells (VWD-AECs) by P-selectin, VWFpp

267 adhesion of neutrophils to LTA-treated human aortic endothelial cells was compromised by gelsolin.

268 nduced adhesion molecule expression in human aortic endothelial cells was dependent on specific struc

269 NO* release from bovine aortic endothelial cells was detected with an NO*-specif

270 ALK1 signaling and VEGF expression in bovine aortic endothelial cells was dose-dependent, that a prog

271 We found that Nox5 activity in bovine aortic endothelial cells was suppressed by two doses of

272 ransfection assays, and untransfected bovine aortic endothelial cells we determined that PKG phosphor

273 Porcine aortic endothelial cells were cultured at confluence on

274 Human umbilical vein and aortic endothelial cells were exposed to laminar shear s

275 Normal and heat-shocked bovine aortic endothelial cells were exposed to normoglycemia (

276 Bovine aortic endothelial cells were incubated with LDL+/-L-4F,

277 In contrast, human aortic endothelial cells were less responsive to oxLDL.

278 Bovine aortic endothelial cells were plated on polyacrylamide g

279 th eNOS Ser-1179 phosphorylation when bovine aortic endothelial cells were stimulated by either a cal

280 When human aortic endothelial cells were stimulated with physiologi

281 tected and atherosusceptible arteries, human aortic endothelial cells were subjected to pulsatile und

282 Rat aortae and cultured rat aortic endothelial cells were treated with Hcy, BT extra

283 Porcine aortic endothelial cells were treated with HMGB1, human

284 When cultured bovine aortic endothelial cells were treated with VEGF (10 ng/m

285 Cultured human aortic endothelial cells were used to assess the differe

286 The labeled hASMCs, along with human aortic endothelial cells, were incorporated into eight T

287 Human monocytes, but not aortic endothelial cells, were responsive to transient (

288 ndothelium but was specifically expressed by aortic endothelial cells where VEGFR2 was found to be ph

289 ced VEGFR2 and Akt phosphorylation in bovine aortic endothelial cells, while PTP1B siRNA increased bo

290 Similar data were obtained in human aortic endothelial cell with NPR-C knockdown.

291 We next transfected bovine aortic endothelial cells with dominant-inhibitory mutant

292 We treated human aortic endothelial cells with exogenous amphiphiles, sho

293 METHODS AND We transfected bovine aortic endothelial cells with N-terminally FLAG-tagged M

294 Treatment of cultured porcine aortic endothelial cells with nitroglycerin (GTN) or 1H-

295 Treatment of bovine aortic endothelial cells with oligosaccharides of hyalur

296 regulator of beta(3)AR signaling in cultured aortic endothelial cells with potentially important impl

297 Stimulation of human aortic endothelial cells with rosiglitazone resulted in

298 We pretreated human aortic endothelial cells with simvastatin for 24 hours,

299 Preincubation of bovine aortic endothelial cells with VEGF (10 ng/ml for 90 min)

300 we show that increased oxidation of FFAs in aortic endothelial cells without added insulin causes in