ライフサイエンスコーパス: neointima

1 increased hyaluronan (HA) deposition in the neointima.

2 l2a1 and Alpl, which localized to the lesion neointima.

3 lar smooth muscle cells within the expanding neointima.

4 h control by measuring degree of stenosis by neointima.

5 g and significantly decreased injury-induced neointima.

6 -positive cells were present within arterial neointima.

7 wed by balloon overstretch of the developing neointima.

8 on in cells of the vascular tunica media and neointima.

9 the regenerating endothelium, but not in the neointima.

10 matrix deposition, and formation of a thick neointima.

11 adventitia and by smooth muscle cells of the neointima.

12 ing for proteomics analysis of the media and neointima.

13 number of SMCs are selected to establish the neointima.

14 ts, with struts being sequestered within the neointima.

15 Insulin-resistant rats developed thicker neointima (0.46+/-0.08 versus 0.37+/-0.06 mm2, P=0.05),

16 ibution of stent struts affect the amount of neointima after SES implantation.

17 manifestation of atherosclerosis in nascent neointima after stenting, associated with adverse events

18 contrast, VSMC-derived cells generating the neointima after vascular injury generally retained the e

19 n in the number of LacZ labeled cells in the neointima after vascular injury, concomitant with reduce

20 rowth factor that is highly expressed in the neointima after vascular injury.

21 bstantial infiltration of macrophages in the neointima and adventitia of the ligated left carotid art

22 ma cells were found in fibrotic areas of the neointima and adventitia.

23 ntial for accumulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the ad

24 -/-)/PSGL-1(-/-) mice also developed smaller neointima and atherosclerotic plaques.

25 opathy samples to assess the role of LMO7 in neointima and fibrosis.

26 Morphometric analysis of the neointima and histopathologic examinations was performed

27 monocyte infiltration in wire injury-induced neointima and in atherosclerotic lesions.

28 sed expression of ETS-1 predominantly in the neointima and overlying endothelium.

29 ession of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas.

30 mia, and CKD stimulates calcification of the neointima and tunica media of the aorta.

31 ha-smooth muscle actin positive cells in the neointima) and endothelial activation (increased P-selec

32 Macrophages infiltrate Nf1(+/-) neointimas, and NF1 patients have increased circulating

33 Four weeks after injury, the neointima area and intima/media ratio were attenuated in

34 ation and proliferative VSMC accumulation in neointima area.

35 vessel area with a decrease in the ratio of neointima area/media + adventitia area (P < 0.05).

36 Neointima arises from smooth muscle cells (SMCs) and not

37 the population of cells within the media and neointima at 7-14 days.

38 s, existing smooth muscle cells give rise to neointima, but on extensive damage, they are replaced by

39 level of p27(kip1) located in the nucleus of neointima cells in SGK-1 knockout mice compared with tha

40 ), and psiepsilonRACK significantly promoted neointima development (32.4+/-4.9%, P=0.033), whereas ep

41 fibrosis, cardiac hypertrophy, and occlusive neointima development.

42 litating reendothelialization and inhibiting neointima development.

43 dation, ApoER2(-/-) mice display exaggerated neointima development.

44 n atherosclerotic plaques and injury-induced neointima did not contain VSMC-derived cells expressing

45 (monocytes, macrophages, lymphocytes) in the neointima did not differ among the different CRPtg genot

46 +) MSC-like cells migrate into the media and neointima during athero- and arteriosclerosis in ApoE(-/

47 sion to 35% of uninjured controls, inhibited neointima formation (>70%), inhibited VSM proliferation

48 ssel remodeling in a mouse model of arterial neointima formation (carotid ligation).

49 ited cell proliferation and markedly reduced neointima formation 14 days post injury; similar results

50 d compound transgenic mice were resistant to neointima formation 21 days after carotid injury and sho

51 RR6 attenuated neointima formation 4 weeks after transplantation.

52 contributing to Mfn-2-mediated prevention of neointima formation after angioplasty.

53 Our method reconstructs 3D neointima formation after arterial injury and allows for

54 t that platelet CD40 plays a pivotal role in neointima formation after arterial injury and might repr

55 However, the direct impact of platelets on neointima formation after arterial injury remains undete

56 let-leukocyte activation and recruitment and neointima formation after arterial injury, potentially t

57 rate of reendothelialization is critical in neointima formation after arterial injury.

58 d contribution of adventitial fibroblasts to neointima formation after balloon angioplasty.

59 Orai3 potential upregulation and role during neointima formation after balloon injury of rat carotid

60 study was to determine the role of Orai1 in neointima formation after balloon injury of rat carotid

61 Herein, we show that neointima formation after carotid artery wire injury red

62 Neointima formation after carotid denudation injury was

63 femoral cuff injury whereas hPBMCs promoted neointima formation after carotid wire injury 4 weeks af

64 nstituted mice, hPBMC reconstitution reduced neointima formation after femoral cuff injury whereas hP

65 in high-fat diet-induced atherosclerosis and neointima formation after injury in atherosclerosis-pron

66 Finally, neointima formation after mechanical arterial injury was

67 BMDCs alone was necessary and sufficient for neointima formation after vascular injury and provide ev

68 Neointima formation after vascular injury is exaggerated

69 y provide strong evidence that asTF promotes neointima formation and angiogenesis in an experimental

70 helial cells of AVFs, leading to accelerated neointima formation and AVF failure.

71 of iPLA(2)beta exacerbates ligation-induced neointima formation and enhanced both production of proi

72 inker protein, was shown to be essential for neointima formation and for p38 mitogen-activated protei

73 mechanisms underlying medial thickening and neointima formation and highlight novel transcriptional,

74 n from media to intima, resulting in reduced neointima formation and increased lumen size.

75 entiviral particles encoding shRNA inhibited neointima formation and inward and outward vessel remode

76 based, paclitaxel-eluting stents on in-stent neointima formation and late incomplete stent apposition

77 w that genetic deficiency of Cxcr7 increased neointima formation and lesional macrophage accumulation

78 Rock1(+/-) to WT BMT led to reduced neointima formation and leukocyte infiltration following

79 NOD treatment significantly reduced neointima formation and neointimal alphaSMA cells.

80 , asTF gene transfer significantly increased neointima formation and neovascularization after carotid

81 ied the effects of Epac1 null by suppressing neointima formation and proliferative VSMC accumulation

82 s as critical cellular effectors of Nf1(+/-) neointima formation and propose a potential therapeutic

83 R2 expression effectively inhibited Nf1(+/-) neointima formation and reduced macrophage content in th

84 scular smooth muscle cells and contribute to neointima formation and repair after acute injury to the

85 rly progression of vascular inflammation and neointima formation and suggest that iPLA(2)beta may rep

86 of IL-1beta signaling in mediating arterial neointima formation and suggest the involvement of IL-1

87 or for the proliferative response underlying neointima formation and target genes trans-activated by

88 ubstrate 2 alpha) in mice profoundly reduces neointima formation and vascular remodelling following c

89 cluding vascular disease, which results from neointima formation and vessel occlusion.

90 Plaque development and excessive neointima formation are hallmarks of atherosclerosis and

91 ed arteries; it also reduced the exaggerated neointima formation at 28 days.

92 ialization at 2 weeks (P<0.01) and increased neointima formation at 4 weeks (P<0.01).

93 rial injury (P<0.05), resulting in decreased neointima formation at 4 weeks compared with control (P<

94 In mice, ETS-DN, but not ETS-MU, reduced neointima formation at days 7 and 21 and reduced the exp

95 Rac1, but not Vav2, also is important for neointima formation but not for hypertension-driven vasc

96 n pathway, suppressed balloon injury-induced neointima formation by 40%.

97 on pathway, in injured arteries also reduced neointima formation by about 40%.

98 on Nf1(+/-) neointima formation, we induced neointima formation by carotid artery ligation in Nf1(+/

99 ARgamma is both necessary and sufficient for neointima formation by components of oxidized low densit

100 suggest that KIS protects against excessive neointima formation by opposing stathmin-mediated VSMC m

101 Neointima formation causes the failure of 60% of arterio

102 odel, Tsc2(+/-) mice significantly increased neointima formation compared with the control mice, and

103 IL8RB-EC, and IL8RA/RB-EC treatment reduced neointima formation dramatically (by 80%, 74%, and 95%)

104 otential of Epac1 as therapeutic targets for neointima formation during vascular remodeling.

105 ole of the human immune system on subsequent neointima formation elicited by vascular injury in a hum

106 Nf1 (Nf1(+/-)) in bone marrow cells enhances neointima formation following arterial injury.

107 f CRP2 enhances VSMC migration and increases neointima formation following arterial injury.

108 f CRP2 enhanced VSMC migration and increased neointima formation following arterial injury.

109 d for NFAT activity, VSMC proliferation, and neointima formation following balloon injury of rat caro

110 proliferation, and also markedly accentuates neointima formation following rat carotid angioplasty.

111 cate that ROCK1 in BM-derived cells mediates neointima formation following vascular injury and sugges

112 phy following monocrotaline and in rats with neointima formation following VEGF receptor blockade and

113 topical application of MCV1 markedly reduced neointima formation in a mouse model of restenosis.

114 ated into injured femoral artery and reduced neointima formation in a mouse model.

115 nvolvement of these transcription factors in neointima formation in a rat carotid artery balloon inju

116 rowth and survival and may contribute to the neointima formation in atherosclerosis and restenosis.

117 ts unveil the role of ETS-1 as a mediator of neointima formation in AVF and may result in the develop

118 d surface, thus suppressing inflammation and neointima formation in balloon-injured rat carotid arter

119 retard development of glomerulosclerosis and neointima formation in chronic transplant dysfunction.

120 Likewise, RNase1 administration reduced neointima formation in comparison with vehicle-treated A

121 n response to injury can result in occlusive neointima formation in diseases such as atherosclerosis

122 which is a signaling axis directly linked to neointima formation in diverse animal models of vasculop

123 We found less balloon injury-induced neointima formation in hyperbilirubinemic Gunn rats and

124 cyte infiltration into the arterial wall and neointima formation in Nf1(+/-) mice.

125 ed arterial injury, we demonstrate decreased neointima formation in NOR1(-/-) mice compared with wild

126 rating decreased cyclin D1 expression during neointima formation in NOR1-deficient mice.

127 At 21 days after ferric chloride injury, neointima formation in P2Y(12)(-/-) arteries was signifi

128 e pathological increases of echogenicity and neointima formation in rats.

129 Neointima formation in response to arterial injury and I

130 4, and Pak1 activities, resulting in reduced neointima formation in response to injury.

131 investigated the role of elevated sCD40L in neointima formation in response to vascular injury in an

132 Remarkably, however, neointima formation in response to vascular injury is pr

133 d demonstrate that NOR1 deficiency decreases neointima formation in response to vascular injury.

134 ollowing this intervention, we found reduced neointima formation in Rock1(+/-) mice compared with tha

135 ima of injured carotid arteries and promotes neointima formation in the comorbid condition of hyperli

136 Neointima formation in the human arterial allografts was

137 Knockout of SGK-1 effectively prevented neointima formation in vein graft.

138 1beta overexpression substantially inhibited neointima formation in vivo and markedly inhibited VSMC

139 roliferation in vitro and for injury-induced neointima formation in vivo by modulating Rac1-NFATc1-cy

140 etermined which cell lineage is critical for neointima formation in vivo in mice.

141 nd proliferation in vitro and injury-induced neointima formation in vivo.

142 motility in vitro and balloon injury-induced neointima formation in vivo.

143 Whether AMPKalpha alters vascular neointima formation induced by vascular injury is unknow

144 Moreover, in a model of neointima formation invoked by carotid artery endothelia

145 ta) is involved in vascular inflammation and neointima formation is largely unknown.

146 gly suggest that the severity of age-related neointima formation is primarily determined by the recip

147 ter treatment of carotids with PDGF and that neointima formation is significantly reduced in carotids

148 media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of

149 ells is sufficient to reproduce the enhanced neointima formation observed in Nf1(+/-) mice when compa

150 led to vascular remodeling characterized by neointima formation over a period of 4 wk.

151 ing VSMC remodeling, and its contribution to neointima formation remain unknown.

152 However, the role of LTC4S in neointima formation remains unknown.

153 e deficient for both ISG12 and NR4A1 exhibit neointima formation similar to wild-type mice.

154 BM-derived FSP-1(+) cells enhance neointima formation through an increase in transendothel

155 of PD0325901 significantly reduced Nf1(+/-) neointima formation to levels of wild-type mice.

156 monstrate that NFATs play a critical role in neointima formation via induction of expression of COX-2

157 Luminal occlusion of the graft caused by neointima formation was 29.3+/-19.4% (n=5) after transfe

158 Neointima formation was associated with up-regulation of

159 Furthermore, neointima formation was dramatically inhibited by lenti-

160 IFN-gammaR-deficient recipients and in which neointima formation was induced by intravenous administr

161 tion compared with the control mice, and the neointima formation was inhibited by treatment with rapa

162 Restenosis and neointima formation were studied with angiography and in

163 unction, invasion of inflammatory cells, and neointima formation were suppressed in mice with heteroz

164 flammatory properties, significantly reduced neointima formation when compared with control.

165 (VEGF)-2 could achieve similar reductions in neointima formation while accelerating, rather than inhi

166 ic SENP1 knockout grafts demonstrate limited neointima formation with attenuated leukocyte recruitmen

167 ling response that was accompanied by severe neointima formation with thickened adventitia.

168 Nox4 inhibits oxidation of SERCA, as well as neointima formation, after ZO common carotid artery inju

169 model, AIP1 deletion in the graft augmented neointima formation, an effect reversed in AIP1/interfer

170 he mechanism by which p38alpha MAPK promotes neointima formation, an in vitro SMC culture system was

171 injury influenced endothelial regeneration, neointima formation, and homing of human inflammatory an

172 arteries had greater intima media thickness, neointima formation, and macrophage content compared wit

173 understanding of the cellular events driving neointima formation, and the molecular pathways that con

174 during the proliferative response underlying neointima formation, and this transcriptional induction

175 aortic graft injury model promotes extensive neointima formation, as shown by optical coherence tomog

176 osis is characterized in part by exaggerated neointima formation, but the underlying mechanism remain

177 nd angiogenic factors in atherosclerosis and neointima formation, emphasizing the problems raised by

178 Strikingly, Nf1+/- mice have increased neointima formation, excessive vessel wall cell prolifer

179 inhibit SMC proliferation and injury-induced neointima formation, induced SMC redifferentiation.

180 SMC p38alpha MAPK activation is required for neointima formation, perhaps because of its ability to p

181 h muscle-specific iPLA(2)beta is involved in neointima formation, we generated transgenic mice in whi

182 gate the role of CCR2 activation on Nf1(+/-) neointima formation, we induced neointima formation by c

183 al role of fbln-5 in vascular remodeling and neointima formation, we induced vascular injury by carot

184 rmine the role of leukocyte-derived ROCK1 in neointima formation, we performed reciprocal bone marrow

185 including inflammatory cell recruitment and neointima formation, were markedly inhibited by PRT06031

186 smooth muscle cells leads to characteristic neointima formation, which can be exacerbated by genetic

187 Injection of wild-type platelets promoted neointima formation, which was associated with increased

188 modeling and identify a pathway required for neointima formation.

189 deling, and in vivo Orai3 knockdown inhibits neointima formation.

190 MC following endoluminal injury and promotes neointima formation.

191 on of Nf1 in myeloid cells is sufficient for neointima formation.

192 ential importance in vascular remodeling and neointima formation.

193 allograft recipients significantly increased neointima formation.

194 injured tissues, preventing inflammation and neointima formation.

195 that ISG12-deficient mice are protected from neointima formation.

196 ation and proliferation resulting in reduced neointima formation.

197 to the luminal surface resulting in reduced neointima formation.

198 ced IFN-gamma-induced VSMC proliferation and neointima formation.

199 STAT3 phosphorylation, MCP-1 expression, and neointima formation.

200 ation and proliferation, 2 critical steps in neointima formation.

201 he plasma membrane recruitment of IQGAP1 and neointima formation.

202 of vascular cells in vein graft, leading to neointima formation.

203 identify mechanisms of mechanical stretch on neointima formation.

204 eir proliferation in the intimal region, and neointima formation.

205 scle cell migration from media to intima and neointima formation.

206 ociated with increased SMC proliferation and neointima formation.

207 , in mediating SMC multiplication leading to neointima formation.

208 outflow reduction without flow cessation or neointima formation.

209 omer proteins in VSMCs and its importance in neointima formation.

210 , WT to Rock1(+/-) BMT resulted in increased neointima formation.

211 tant role for DDAH in EC regeneration and in neointima formation.

212 e settings of postangioplasty and thereby in neointima formation.

213 migration from media to intima and decreased neointima formation.

214 roliferation in intima, resulting in reduced neointima formation.

215 owth and motility and balloon injury-induced neointima formation.

216 oliferation and prevents atherosclerosis and neointima formation.

217 re, we examined the role of IL-1 in arterial neointima formation.

218 se of graft failure caused by thrombosis and neointima formation.

219 in-converting enzyme inhibitors that prevent neointima formation.

220 tion and proliferation, resulting in reduced neointima formation.

221 OCs, proliferation, and migration leading to neointima formation.

222 muscle cells are the primary contributors to neointima formation.

223 migration, and injury-induced vascular wall neointima formation.

224 tetheinase activity, is possibly involved in neointima formation.

225 R2 antagonist significantly reduced Nf1(+/-) neointima formation.

226 s, resulting in either minimal or aggravated neointima formation.

227 ic retinopathy, whereas lincRNA-p21 controls neointima formation.

228 MT, deposition of fibronectin, and increased neointima formation.

229 Akt signaling to promote VSMC migration and neointima formation.

230 nti-inflammatory properties, and it prevents neointima formation.

231 ch as hypertension, arterial remodeling, and neointima formation.

232 of dysfunction, in part because of excessive neointima formation.

233 he aberrant pathway responsible for enhanced neointima formation.

234 Entire 3D neointima formations with different geometries were obse

235 Neointima-forming mechanisms are controversial but possi

236 SMCs newly migrated to the neointima had increased division defects and increased a

237 al wire injury model was used for studies of neointima hyperplasia and arterial stenosis.

238 of AMPKalpha in the development of vascular neointima hyperplasia and to elucidate the underlying me

239 odel of vascular injury, we observed reduced neointima hyperplasia in Quaking viable mice, which have

240 amined the role of ETS-1 in the formation of neointima in AVF.

241 Histopathology demonstrated the presence of neointima in both SIS and PTFE.

242 et, FSP-1, for preventing the development of neointima in vein grafts.

243 rterial injury and IGF-1R phosphorylation in neointima increased significantly in LAR(-/-) mice compa

244 nly genome-wide association studies of human neointima-induced in-stent stenosis confirmed the associ

245 The structure-activity relationship for neointima induction by LPA analogs in vivo is identical

246 d CamKIIdelta2 upregulation in the media and neointima; inhibited cell proliferation and markedly red

247 Development of the neointima into a typical atherosclerotic lesion and cons

248 oth Muscle Cell (VSMC) migration into vessel neointima is a therapeutic target for atherosclerosis an

249 If SMC evade this first barrier and neointima is formed, A20 has a therapeutic potential by

250 In this setting, neointima is more prone to become lipid laden and develo

251 cytoplasmic abundance within the intima and neointima layers.

252 Lack of resolution of the pathologic neointima leads to stenosis, tissue ischemia, and organ

253 Maximum consecutive lipid neointima length was shorter in DES than in BMS (2.4 [1.

254 of the smooth muscle cells captured from the neointima lesion by laser capture microdissection at 16

255 ry system produces substantial mitigation of neointima, likely due to its favorable physical properti

256 presence of large necrotic cores within the neointima may be associated with the inability of the ve

257 IL-1beta(-/-) mice had reduced neointima/media compared to wild-type (P < 0.05), wherea

258 1(+/+) marrow both had significantly reduced neointima/media compared with IL-1R1(+/+) to IL-1R1(+/+)

259 aneous IL-1ra also had significantly reduced neointima/media compared with placebo (P < 0.05).

260 The neointima/media of mice deficient in the IL-1 signaling

261 /+) (P < 0.05) but had significantly greater neointima/media than IL-1R1(-/-) to IL-1R1(-/-) controls

262 modeled pulmonary arteries, ie, endothelium, neointima, medial smooth muscle, and adventitia, in the

263 These, in turn, impact on neointima (NI) formation (vascular smooth muscle cell [V

264 rafts fail within 10 years after CABG due to neointima (NI) formation, a process involving the prolif

265 Epac1 gene led to a significant reduction in neointima obstruction in response to vascular injury.

266 ve coronary angiography, with an increase in neointima of 0.68+/-0.43 mm(2) on optical coherence tomo

267 SCPEP1 protein is highly expressed in the neointima of 2 models of vascular remodeling.

268 g coronary vessels, LPP was expressed in the neointima of cells lacking smoothelin and showed express

269 munohistochemistry revealed human CRP in the neointima of CRPtg, but little or none was observed in t

270 lating calcification were upregulated in the neointima of drug-eluting stents.

271 hondromyocytes," were also identified in the neointima of human coronary arteries.

272 pregulated by myocardin and expressed in the neointima of injured aorta.

273 ifferentiate into smooth muscle cells in the neointima of injured arteries, we hypothesized that the

274 In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and promotes neoin

275 In neointima of normolipidemic animals, TF and active caspa

276 rated increased heparanase expression in the neointima of obese, hyperlipidemic rats in comparison to

277 n-like protein (ESDN) is up-regulated in the neointima of remodeling arteries and modulates vascular

278 rate through an irradiated vein graft to the neointima of the vessel and transdifferentiate to expres

279 via low density lipoprotein retention in the neointima of vessels due to binding with modified proteo

280 a novel gene expressed in the adventitia and neointima on arterial injury and found that it functiona

281 The presence of lipid-laden neointima or calcification inside the stents was defined

282 In conclusion, CaMKII stimulates neointima proliferation after vascular injury by regulat

283 association with T-cadherin protects against neointima proliferation and atherosclerosis.

284 Neointima size was further reduced in vessels treated wi

285 dothelialization and significantly increased neointima size.

286 e extent of heparanase expression within the neointima strongly correlated with the neointimal thickn

287 The targeted NP group resulted in lower neointima-to-media (N/M) scores at 2 wk versus control g

288 Carotid artery neointima was induced by ligation, and arteries were har

289 Surface neointima was quantified 2 and 4 weeks after transplanta

290 hich cell types contribute to the developing neointima, we established a novel mouse model of resteno

291 tidylinositol 3-kinase signaling in Nf1(+/-) neointimas, we tested the hypothesis that Ras-Erk signal

292 Neoatherosclerosis and lipid neointima were more frequently observed and had more lon

293 Young aortas invariably developed thicker neointima when transplanted into old recipients than whe

294 em/progenitor cells exists within developing neointima, which displays the ability to differentiate i

295 -) mice resulted in accelerated formation of neointima, which is composed predominantly of VSMCs.

296 /- mice resulted in accelerated formation of neointima, which is composed predominantly of VSMCs.

297 of lipid-laden foamy macrophages within the neointima with or without necrotic core formation.

298 id ligation, C57Bl/6 mice developed a marked neointima with robust CaMKII protein expression.

299 men at postprocedure rather than exaggerated neointima within the stent or plaque proliferation at th

300 Therapies targeting the neointima would represent a significant advance in PAH t