ライフサイエンスコーパス: aortic smooth muscle cell

1 icaprost-induced IP internalization in human aortic smooth muscle cells.

2 verse cholesterol transport (RCT) from human aortic smooth muscle cells.

3 F) binding to heparan sulfate (HS) on bovine aortic smooth muscle cells.

4 ng either receptor alone, or in IP-deficient aortic smooth muscle cells.

5 d apo, APOE, inhibit S-phase entry of murine aortic smooth muscle cells.

6 on and NPR-A gene expression in cultured rat aortic smooth muscle cells.

7 -kinase-Akt cascade and Ras-MAPK pathways in aortic smooth muscle cells.

8 to modulate leukocyte binding to colonic and aortic smooth muscle cells.

9 A promoter in primary and established rodent aortic smooth muscle cells.

10 agments increased the proliferation of human aortic smooth muscle cells.

11 mediated MMP production from cultured rabbit aortic smooth muscle cells.

12 n NO-induced cell motility in differentiated aortic smooth muscle cells.

13 uces activation of protein kinase D (PKD) in aortic smooth muscle cells.

14 NO-stimulated motility in differentiated rat aortic smooth muscle cells.

15 died transcription of the IGF-1R gene in rat aortic smooth muscle cells.

16 eceptor (VLDL), and apoE receptor-2 in mouse aortic smooth muscle cells.

17 d that PDGF increased HETE levels in porcine aortic smooth muscle cells.

18 imulated PKA in a cAMP-independent manner in aortic smooth muscle cells.

19 rly C5b-9, induces cell cycle progression in aortic smooth muscle cells.

20 ld be controlled by O-GlcNAcylation in human aortic smooth muscle cells.

21 vs. 0.6% +/- 0.2% control, p < 0.001) of rat aortic smooth muscle cells.

22 n a time- and dose-dependent manner in human aortic smooth muscle cells.

23 active MMP-2 from elastase-treated male rat aortic smooth muscle cells.

24 ividual hyperpermeable ferret portal vein or aortic smooth muscle cells.

25 ofile of mechanically induced genes in human aortic smooth muscle cells.

26 donors inhibit the migration of subcultured aortic smooth muscle cells.

27 few genes are mechanically induced in human aortic smooth muscle cells.

28 omegalovirus immediate early promoter in rat aortic smooth muscle cells.

29 a transient and dose-dependent manner in rat aortic smooth muscle cells.

30 nthesis and cell replication in cultured rat aortic smooth muscle cells.

31 or BB) were also observed in cultured bovine aortic smooth muscle cells.

32 xLDL and HA production in vitro, using human aortic smooth muscle cells.

33 1-C did inhibit proliferation by primary rat aortic smooth muscle cells.

34 II (Ang II) on MCP-1 gene expression in rat aortic smooth muscle cells.

35 m readily infected rabbit, bovine, and human aortic smooth muscle cells.

36 by growth factor stimulation in cultured rat aortic smooth muscle cells.

37 herosclerosis involving the proliferation of aortic smooth muscle cells.

38 an umbilical vein endothelial cells or human aortic smooth muscle cells.

39 no effect on Cu/Zn SOD mRNA levels in human aortic smooth muscle cells.

40 ent reductions in viability in rat and human aortic smooth muscle cells.

41 ophages, several endothelial cell lines, and aortic smooth muscle cells.

42 to platelet-derived growth factor-BB in rat aortic smooth muscle cells.

43 attenuates 7-KC-induced cell death in human aortic smooth muscle cells.

44 echanisms of S100A12-mediated dysfunction of aortic smooth muscle cells.

45 n of new elastic fibers in cultures of human aortic smooth muscle cells.

46 ed pathways were studied in cultured primary aortic smooth muscle cells.

47 lotho expression in human arteries and human aortic smooth muscle cells.

48 ondroitin sulfate synthesis in primary human aortic smooth muscle cells.

49 pressed individually or together in A7r5 rat aortic smooth muscle cells.

50 -cell KATP currents recorded in isolated rat aortic smooth muscle cells.

51 gene expression in both 10T1/2 cells and rat aortic smooth muscle cells.

52 diovascular (patho)physiology, primary human aortic smooth muscle cells.

53 ic transdifferentiation and calcification of aortic smooth muscle cells.

54 extracellular matrix elastin and collagen by aortic smooth muscle cells.

55 inhibited serum-stimulated proliferation of aortic smooth-muscle cells.

56 )R) densities in transiently transfected rat aortic smooth muscle cells (A10 cells) and stably transf

57 Ca2+ signaling was also observed in cultured aortic smooth muscle cells (A10 cells).

58 ced glycation end products (RAGE), in murine aortic smooth muscle cells abolished cytokine-augmented

59 In cultured mouse aortic smooth muscle cells, ACLP mRNA and protein were u

60 tment (for 1 h) of murine macrophages or rat aortic smooth muscle cells (activated with endotoxin) wi

61 oteomics analysis of the secretome of murine aortic smooth muscle cells, after miR-195 manipulation,

62 on by small interfering RNA in primary human aortic smooth muscle cells also potently inhibited ROS p

63 plete loss of alpha(1D)-AR function in mouse aortic smooth muscle cells and abrogation of alpha(1D)-A

64 r defects due to this ACTA2 mutation in both aortic smooth muscle cells and adventitial fibroblasts m

65 Primate aortic smooth muscle cells and adventitial fibroblasts w

66 2) inhibited ADAMTS-5 expression in isolated aortic smooth muscle cells and blocked the spontaneous r

67 In primary cultures of aortic smooth muscle cells and C2C12 cells, the insulin-

68 CX3CR1 is expressed on human aortic smooth muscle cells and CX3CR1/apolipoprotein E d

69 differentiation and calcification by ank/ank aortic smooth muscle cells and explants were corrected b

70 thelial cell mitogen, but anti-mitogenic for aortic smooth muscle cells and fibroblasts when acting v

71 GFRP mRNA is constitutively expressed in rat aortic smooth muscle cells and further induced by treatm

72 MP-9 expression in both primary cultured rat aortic smooth muscle cells and in a smooth muscle cell l

73 Similar results were detected in human aortic smooth muscle cells and in vivo using mice overex

74 tection induced by OA-NO(2) in both cultured aortic smooth muscle cells and in vivo.

75 ion enhanced RGC-32 mRNA expression in human aortic smooth muscle cells and induced nuclear transloca

76 tivity in nuclear proteins obtained from rat aortic smooth muscle cells and macrophages stimulated wi

77 Accumulated HA stimulated migration of aortic smooth muscle cells and monocyte adhesiveness to

78 her atherosclerosis-associated cathepsins in aortic smooth muscle cells and monocytes.

79 of ALDH2 using immortalized ALDH2-deficient aortic smooth muscle cells and mouse aortas with selecti

80 ety of normal human endothelial cells and in aortic smooth muscle cells and reduce culture requiremen

81 F-I) increases elastin gene transcription in aortic smooth muscle cells and that this up-regulation i

82 H oxidase-dependent superoxide generation by aortic smooth muscle cells and their consequent prolifer

83 nors on migration of primary cultures of rat aortic smooth muscle cells and to compare and contrast t

84 infected endothelial cells, fibroblasts, and aortic smooth muscle cells and to compare these profiles

85 s was performed on two cell lines: A7r5 (rat aortic smooth muscle cells) and SH-SY5Y (human neuroblas

86 g gene expression profiling of mouse primary aortic smooth muscle cells, and confirming the results b

87 s highly expressed in human coronary artery, aortic smooth muscle cells, and in human arterial and ve

88 vity against cell lines such as HUVEC, human aortic smooth muscle cells, and MRC5 lung fibroblasts.

89 se reporter activity in primary cultured rat aortic smooth muscle cells, and this activity was not de

90 Finally, in human aortic smooth muscle cells, angiotensin II moderately in

91 t A10 VSMCs and in primary cultures of human aortic smooth muscle cells (AoSMCs) at low nanomolar con

92 gration were reduced in Gucy1a3(-/-) primary aortic smooth muscle cells (AoSMCs), and proliferation w

93 In rat primary aortic smooth muscle cells, apelin inhibited Ang II-medi

94 on other anchorage-dependent cell lineages, aortic smooth muscle cells are found to spread and organ

95 ased protein glutathiolation in COS-7 or rat aortic smooth muscle cells as detected by anti-protein g

96 ansmembrane chemokine, is expressed in human aortic smooth muscle cell (ASMC).

97 ed that the chemokine CXCL16 is expressed in aortic smooth muscle cells (ASMC) and induces ASMC adhes

98 Cultured aortic smooth muscle cells (ASMC) from Watanabe heritabl

99 2-fold higher in aortas, tail arteries, and aortic smooth muscle cells (ASMCs) obtained from adult m

100 lamp electrophysiology shows that in porcine aortic smooth muscle cells, ATP stimulates an inward cur

101 For example, in aortic smooth muscle cells B-Myb represses transcription

102 ve characterized the calcification of bovine aortic smooth muscle cell (BASMC) cultures in vitro and

103 Bovine aortic smooth muscle cell (BASMC) cultures undergo miner

104 (2)III, was evident in IP/TPalpha-HEK and in aortic smooth muscle cells, but not in cells expressing

105 riptional activity in A7r5 or primary canine aortic smooth muscle cells, but show little activity in

106 vitro, NOD inhibited proliferation of human aortic smooth muscle cells by causing a G1-arrest and pr

107 conclude that PGI2 inhibits proliferation of aortic smooth muscle cells by coordinately blocking CRE-

108 ow that sGC can be S-nitrosylated in primary aortic smooth muscle cells by S-nitrosocysteine (CSNO),

109 We found that HAS2, the main synthase in aortic smooth muscle cells, can be O-GlcNAcylated on ser

110 n inhibited increased proliferation of human aortic smooth muscle cells caused by glucose.

111 Here we show that UCP1 expression in aortic smooth muscle cells causes hypertension and incre

112 Proliferation of aortic smooth muscle cells contributes to atherogenesis

113 In primary aortic smooth muscle cell cultures, we found that S100A1

114 mental differences among different models of aortic smooth muscle cell cultures.

115 Indeed, we found that HDL and APOE suppress aortic smooth muscle cell cycle progression by stimulati

116 The viability of rat aortic smooth muscle cells decreased within 3 h of treat

117 Dab2 in NIH3T3 mouse fibroblasts and A10 rat aortic smooth muscle cells demonstrates that its express

118 In addition, aortic smooth muscle cells derived from A2bAR KO mice di

119 lt ventricular cardiomyocytes but not in rat aortic smooth muscle cells, endothelial cells, or cardia

120 The kinetics of sterol efflux from human aortic smooth muscle cells equilibrated with a [(3)H]ben

121 rimary cultures of chr4(Delta70kb/Delta70kb) aortic smooth muscle cells exhibited excessive prolifera

122 tracts prepared from primary cultures of rat aortic smooth muscle cells exhibited specific USF1 and U

123 ters the motogenic phenotype of cultured rat aortic smooth muscle cells exposed to NO from inhibition

124 La cells overexpressing ET1 receptors and in aortic smooth muscle cells expressing endogenous levels

125 (2.5-10 microm) of GD3, incubated with human aortic smooth muscle cells for a short period of time (1

126 Insulin increased VEGF mRNA levels in mouse aortic smooth muscle cells from 10(-9) to 10(-7) m with

127 ficantly lower in aortic tissue and cultured aortic smooth muscle cells from BAV patients compared wi

128 timulated signaling events and growth in the aortic smooth muscle cells from normal and hyperglycemic

129 kinase p44MAPK to phosphorylated p44MAPK in aortic smooth muscle cells from rabbit or human origin.

130 ed VLDL binding and uptake in vitro in mouse aortic smooth muscle cells from SM22alpha-TFPI and wild-

131 Mouse aortic smooth muscle cells from SM22alpha-TFPI mice demo

132 Isolated aortic smooth muscle cells from the Rgs5(-/-) mice exhib

133 To determine the role of SAA on aortic smooth muscle cell gene expression, a preliminary

134 2.5 micromol/L, significantly stimulated rat aortic smooth muscle cell growth as determined by cell c

135 Recombinant TFPI had no effect on human aortic smooth muscle cell growth but inhibited platelet-

136 ant lipid peroxidation products, induces rat aortic smooth muscle cell growth through redox-sensitive

137 effects of 4-hydroxy-2-nonenal (HNE) on rat aortic smooth muscle cell growth.

138 transcription-polymerase chain reaction from aortic smooth muscle cells had 100% identity throughout

139 Primary human aortic smooth muscle cells (HAoSMCs) were genotyped for

140 In human aortic smooth muscle cells (HAoSMCs), aldosterone dose-d

141 inducing migration of VEGFR2-negative human aortic smooth muscle cells (hAOSMCs), and this induction

142 Similarly, in primary human aortic smooth muscle cells (HAoSMCs), NH4Cl treatment re

143 ed the role of NFATc1 in MCP-1-induced human aortic smooth muscle cell (HASMC) growth and migration a

144 examined whether minocycline inhibited human aortic smooth muscle cell (HASMC) migration induced by v

145 g pathway associated with MCP1-induced human aortic smooth muscle cell (HASMC) migration.

146 export and degradation in facilitating human aortic smooth muscle cell (HASMC) proliferation.

147 nsduction pathways elicited by CXCL16, human aortic smooth muscle cells (HASMC) were treated with pha

148 ilical vein endothelial cells (HUVEC), human aortic smooth muscle cells (HASMC), A549 (human lung car

149 We have found that human aortic smooth muscle cells (HASMCs) and human umbilical

150 In addition, studies on human aortic smooth muscle cells (HASMCs) demonstrated membran

151 Cultured human aortic smooth muscle cells (HASMCs) exhibited constituti

152 ced Pak1 phosphorylation/activation in human aortic smooth muscle cells (HASMCs) in a delayed time-de

153 ndothelial cell types such as cultured human aortic smooth muscle cells (HASMCs) lack the ability to

154 inding to alpha(v)beta(3) integrins on human aortic smooth muscle cells (HASMCs) or human umbilical v

155 in were increased by 2- to 3.5-fold in human aortic smooth muscle cells (HASMCs) treated with PDGF (2

156 Human aortic smooth muscle cells (hASMCs) were labeled with ul

157 Human aortic smooth muscle cells (HASMCs) were stimulated with

158 In vitro, knockdown of T-cadherin from human aortic smooth muscle cells (HASMCs) with synthetic pheno

159 ted T cells (NFAT)-dependent manner in human aortic smooth muscle cells (HASMCs), and blockade of NFA

160 of contractile markers in co-cultured human aortic smooth muscle cells (HASMCs).

161 mRNA and protein were investigated in human aortic smooth muscle cells (HASMCs).

162 hoGEF or leukemia-associated RhoGEF in human aortic smooth muscle cells (HASMCs).

163 uced anti-apoptotic effect in cultured human aortic smooth muscle cells (HASMCs).

164 PDE5A mRNA is expressed in aortic smooth muscle cells, heart, placenta, skeletal mu

165 n umbilical vein endothelial cells (HUVECs), aortic smooth muscle cells, HeLa cells, HEK293 cells, an

166 inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization

167 d inhibit fibronectin matrix assembly by rat aortic smooth muscle cells, HUASMCs, A7r5 cells, IMR-90

168 ed DNA synthesis and proliferation in normal aortic smooth muscle cells (IC50, 23.2+/-3.8 and 23.6+/-

169 TGF increased collagen synthesis in cultured aortic smooth muscle cells in a dose- and time-dependent

170 e pulmonary artery endothelial cells and rat aortic smooth muscle cells in a time- and dose-dependent

171 inhibited proliferation and migration of rat aortic smooth muscle cells in culture by 45 and 60%, res

172 n2+ influx with fura-2 fluorometry in rabbit aortic smooth muscle cells in primary culture were desig

173 In transient transfection assays in rat aortic smooth muscle cells in primary culture, 5 kilobas

174 TSP-1 expression in glucose-stimulated human aortic smooth muscle cells in vitro.

175 one receptors were detected in human and rat aortic smooth muscle cells in vivo and in vitro (in subc

176 Forced expression of MLC(17a) in aortic smooth muscle cells increased (p < 0.05) the rate

177 dothelial cells but inhibits growth of human aortic smooth muscle cells induced by platelet-derived g

178 Similarly, TGFbeta1 treatment of human aortic smooth muscle cells induced SM actin, calponin1,

179 determined that (1) GTN treatment of primary aortic smooth muscle cells induces S-nitrosylation of sG

180 e heme oxygenase-1 (ho-1) gene by hypoxia in aortic smooth muscle cells is mediated by hypoxia-induci

181 Migration of aortic smooth muscle cells is thought to be of essential

182 ay on VEGF expression was confirmed in mouse aortic smooth muscle cells isolated from insulin recepto

183 his age-dependent defect in VEGF expression, aortic smooth muscle cells isolated from young rabbits (

184 ndoleamine 2,3-dioxygenase (IDO) activity in aortic smooth muscle cells, leading to a marked inhibiti

185 rgic activation of 5-HT(2A) receptors in rat aortic smooth muscle cells leads to an increase in intra

186 n of ALDH2 in the cytosol of ALDH2-deficient aortic smooth muscle cells led to a significant increase

187 endothelial cells, NIH 3T3 cells, or the rat aortic smooth muscle cell line A7r5.

188 bility by using A7r5 cells, an embryonic rat aortic smooth muscle cell line that coexpresses Cxs 43 a

189 PKCbeta gene expression in A10 cells, a rat aortic smooth muscle cell line.

190 we demonstrated in vitro that human newborn aortic smooth muscle cell lines can contract and adhere

191 ypothesis that an increased PDE3 activity in aortic smooth muscle cells may contribute to accelerated

192 In primary murine aortic smooth muscle cells, mDia1 is required for recept

193 In vitro, SPM treatment inhibited mouse aortic smooth muscle cell migration (IC(5)(0) congruent

194 ophages as well as their survival, promoting aortic smooth muscle cell migration and cytokine product

195 with AdRZ also reduced PDGF-induced porcine aortic smooth muscle cell migration by approximately 50%

196 latelet-derived growth factor-stimulated rat aortic smooth muscle cell migration.

197 ltage-sensitive calcium currents in A7r5 rat aortic smooth muscle cells (native KCNQ currents or over

198 In human aortic smooth muscle cells, neither prevention of SOCS-3

199 ectrophoretic mobility shift assays with rat aortic smooth muscle cell nuclear extracts, Sp1 and Sp3

200 ctivation of the ERK 1/2(MAPK) system in rat aortic smooth muscle cells occurs through specific integ

201 ated metallothionein expression in ascending aortic smooth muscle cells of BAV patients that may cont

202 stimulates chemotaxis of both human and rat aortic smooth muscle cells on gelatin-coated filters.

203 Infection of ALDH2-deficient aortic smooth muscle cells or isolated aortas with adeno

204 hrough endogenous Kv7.5 channels in A7r5 rat aortic smooth muscle cells or through Kv7.4/Kv7.5 hetero

205 In cultured rat aortic smooth muscle cells, overexpression of FRNK atten

206 induced tissue factor gene expression in rat aortic smooth muscle cells; oxidized low density lipopro

207 In rat aortic smooth muscle cells, PDTC induced cell shrinkage,

208 In cultured human aortic smooth muscle cells, pharmacologic or genetic act

209 A cloned subpopulation of bovine aortic smooth muscle cells previously shown capable of o

210 ce in regard to the potential role of GD3 in aortic smooth muscle cell proliferation and apoptosis th

211 The prostanoid prostacyclin (PGI2) inhibits aortic smooth muscle cell proliferation by blocking cell

212 The nanoparticles inhibited human aortic smooth muscle cell proliferation in vitro and sho

213 t lactosylceramide (LacCer) stimulated human aortic smooth muscle cell proliferation via specific act

214 In human aortic smooth muscle cells, prostaglandin E2 (PGE2) stim

215 isms by which nitric oxide (NO) inhibits rat aortic smooth muscle cell (RASMC) proliferation.

216 mRNA and protein expression in cultured rat aortic smooth muscle cells (RASMC) by increasing gene tr

217 Rat aortic smooth muscle cells (RASMC) contain constitutive

218 , and compartmentation of AC isoforms in rat aortic smooth muscle cells (RASMC).

219 ferative effects of nitric oxide (NO) on rat aortic smooth muscle cells (RASMC).

220 without affecting cognate mRNA levels in rat aortic smooth muscle cells (RASMC).

221 to the contractile phenotype in cultured rat aortic smooth muscle cells (RASMC).

222 sonoporation transfection efficiency in rate aortic smooth muscle cells (RASMCs) of 6.9%+/-2.2% (n=9)

223 of nitrite plus nitrate was observed in rat aortic smooth muscle cells (RASMCs) stably transfected w

224 cts of oleic acid on primary cultures of rat aortic smooth muscle cells (RASMCs) were studied.

225 n of FGFR-1 stimulates OPN expression in rat aortic smooth muscle cells (RASMCs), explored the signal

226 o ERK1/2 activation and DNA synthesis in rat aortic smooth muscle cells (RASMCs).

227 timulated proliferation and migration of rat aortic smooth muscle cells (RASMCs).

228 eased VCAM-1 mRNA expression in cultured rat aortic smooth muscle cells (RASMCs).

229 umor necrosis factor (TNF)-alpha treated rat aortic smooth muscle cells (RASMCs).

230 f Ca(2+) on whole-cell K(ATP) current in rat aortic smooth muscle cells recorded in a physiological [

231 ion of 50 microM ATP, all individual porcine aortic smooth muscle cells respond with rapid rises from

232 itamin D receptor activators conferred human aortic smooth muscle cells responsive to FGF-23 signalin

233 renergic receptor (AR) associated with human aortic smooth muscle cells resulted in a dose- and time-

234 of chicken embryo fibroblasts (CEF) and rat aortic smooth muscle cells (RSM) with dsSIN:C3 caused cy

235 CADTK expression in a mesenchymal cell, rat aortic smooth muscle cells (RSMC).

236 gs, rosiglitazone and pioglitazone, on human aortic smooth muscle cell (SMC) expression of insulin-li

237 Here, we examined the effects of GTPs on aortic smooth muscle cell (SMC) proliferation.

238 K1 and ERK1/2 co-immunoprecipitated from rat aortic smooth muscle cells (SMC) plated on fibronectin,

239 sly reported that the induction of JE in rat aortic smooth muscle cells (SMC) was specific to platele

240 Confluent, growth-arrested rat aortic smooth muscle cells (SMC) were transiently transf

241 dependent manner compared with 5.5 mM in rat aortic smooth muscle cells (SMC).

242 herosclerotic plaque, macrophages, and human aortic smooth muscle cells (SMC).

243 KA activators regulate osteoclastogenesis in aortic smooth muscle cells (SMC).

244 O donors and cGMP analogues on the growth of aortic smooth muscle cells (SMCs) derived from newborn,

245 Here we report that bovine aortic smooth muscle cells (SMCs) express A-myb.

246 est this hypothesis more rigorously, we used aortic smooth muscle cells (SMCs) from mice lacking COMT

247 ta-aminopropionitrile (BAPN) in cultured rat aortic smooth muscle cells (SMCs) reduced the chemotacti

248 in heavy chain (SM-MHC) gene in cultured rat aortic smooth muscle cells (SMCs) required the presence

249 Mouse aortic smooth muscle cells (SMCs) were loaded for 72 h w

250 In human aortic smooth muscle cells (SMCs), IGF-1 rapidly increas

251 in D3-upregulated protein (VDUP)-1, in human aortic smooth muscle cells (SMCs).

252 th muscle (SM) alpha-actin expression in rat aortic smooth muscle cells (SMCs).

253 togenesis and proliferation rate of cultured aortic smooth-muscle cells (SMCs) and skin fibroblasts f

254 tion (7-fold compared with control) in human aortic smooth muscle cells specifically by activating me

255 -dihydroxynonene (GS-DHN) to cultures of rat aortic smooth muscle cells stimulated protein kinase C,

256 tured iNOS(-/-) versus iNOS-expressing mouse aortic smooth muscle cells, suggesting that iNOS-derived

257 ofile of mechanically induced genes in human aortic smooth muscle cells suggests a response of defens

258 tic tissue and in primary cultures of murine aortic smooth muscle cells supported these findings.

259 ed on the cell surface when expressed in rat aortic smooth muscle cells that express no endogenous AR

260 c pathway activated by high glucose in human aortic smooth muscle cells that mediates up-regulation o

261 In this study, we show in rat aortic smooth muscle cells that PDGF-BB down-regulated p

262 cient activation of the cyclin A promoter in aortic smooth muscle cells, that the CRE is primarily oc

263 between S100A12 expression and apoptosis of aortic smooth muscle cells, this study identifies novel

264 Exposure of human aortic smooth muscle cells to 7-KC increased autophagic

265 Overexpression of RGC-32 induced quiescent aortic smooth muscle cells to enter S-phase.

266 a pivotal role in the response of ascending aortic smooth muscle cells to oxidative stress cues norm

267 tudy examined the response of cultured human aortic smooth muscle cells to varying levels of extracel

268 Male and female rat aortic smooth muscle cells treated with elastase for 1,

269 Human and rat aortic smooth muscle cells treated with simvastatin show

270 RNA isolated from cultured human aortic smooth muscle cells treated with tumor necrosis f

271 d not affect that of umbilical vein or human aortic smooth muscle cells, trophoblasts, fibroblasts, o

272 tify the targets of S-nitrosylation in human aortic smooth muscle cells upon exposure to S-nitrosocys

273 ed to fibroblasts as it was also observed in aortic smooth muscle cells upon silencing NPC2 gene by s

274 Experiments were performed with aortic smooth muscle cells using inhibitor screening, sm

275 Reduction of S100A12 expression in human aortic smooth muscle cells using small hairpin RNA atten

276 The adverse effects of PGE2 on aortic smooth muscle cell viability and cytokine secreti

277 The presence of SmLIM expression within aortic smooth muscle cells was confirmed by in situ hybr

278 ostaglandin E(2) (PGE(2)) release from human aortic smooth muscle cells was examined.

279 In a screen of proteins expressed in human aortic smooth muscle cells, we identified a novel gene p

280 Moreover, under control conditions, when rat aortic smooth muscle cells were dialyzed with either cyc

281 Rat aortic smooth muscle cells were incubated with engineere

282 role of endogenously produced H(2)O(2), rat aortic smooth muscle cells were infected with adenoviral

283 Human aortic smooth muscle cells were irradiated with gamma ra

284 Mesangial cells, fibroblasts, and aortic smooth muscle cells were isolated from SPARC-null

285 In vitro analyses of human aortic smooth muscle cells were performed to test the ef

286 Primary aortic smooth muscle cells were significantly activated

287 hains on elastogenesis in blood vessels, rat aortic smooth muscle cells were transduced with a GAG-de

288 lated by cAMP-dependent phosphorylation, rat aortic smooth muscle cells were treated in vivo with cAM

289 Confluent rat aortic smooth muscle cells were treated with OxyHb in a

290 ession and proliferation of cultured primary aortic smooth muscle cells, whereas high-molecular-weigh

291 ell adhesion and soluble factors both in rat aortic smooth muscle cells, which express endogenous Pyk

292 Treatment of wild-type mouse aortic smooth muscle cells with 8-Br-cGMP also induced t

293 The incubation of primary mouse aortic smooth muscle cells with apoE3 resulted in dose-d

294 terventions: In vitro: a) Stimulation of rat aortic smooth muscle cells with bacterial lipopolysaccha

295 Stimulation of rat aortic smooth muscle cells with bacterial LPS and gamma-

296 Treatment of quiescent rat aortic smooth muscle cells with either alpha-thrombin or

297 ductus deferens (DDT1MF-2) cells and porcine aortic smooth muscle cells with either mannitol (50 mM)

298 Upon treatment of primary rat aortic smooth muscle cells with hydrogen peroxide, we ob

299 Treatment of rat aortic smooth muscle cells with the NO donors, sodium ni

300 Treatment of human aortic smooth muscle cells with thrombin increased DNA s