ライフサイエンスコーパス: vascular wall

1 ies compromise interactions with the damaged vascular wall.

2 an antiatherogenic lipid environment in the vascular wall.

3 ing monocytes to the injured atherosclerotic vascular wall.

4 ateral induction throughout the width of the vascular wall.

5 ively regulating monocyte recruitment to the vascular wall.

6 elium, inhibiting their migration across the vascular wall.

7 ovel Rac1-dependent signaling pathway in the vascular wall.

8 mulation of fluorescent myeloid cells in the vascular wall.

9 ects of vascular 5-MTHF from homocysteine on vascular wall.

10 zed as an inflammatory disease involving the vascular wall.

11 -- a potential mechanism for adhesion to the vascular wall.

12 ion and fibroproliferative remodeling in the vascular wall.

13 Th1 subset and recruits macrophages into the vascular wall.

14 ncy drastically reduced levels of eNO in the vascular wall.

15 drenergic modulation of eNOS pathways in the vascular wall.

16 ng vascular development and within the adult vascular wall.

17 is essential to maintain homeostasis of the vascular wall.

18 ched beta-actin-expressing endothelia in the vascular wall.

19 nflammatory and proliferative changes in the vascular wall.

20 in axis, which is different from that in the vascular wall.

21 al lining to its surrounding matrices in the vascular wall.

22 r regulation of NO signaling pathways in the vascular wall.

23 ress, which might instead be confined to the vascular wall.

24 determinant of NO-dependent signaling in the vascular wall.

25 events inappropriate apoptotic damage to the vascular wall.

26 nt to impair function of cells composing the vascular wall.

27 the pathogenesis of several disorders of the vascular wall.

28 o amplify high-glucose-induced injury in the vascular wall.

29 results from passive lipid deposition in the vascular wall.

30 cular smooth muscle cells (VSMCs) within the vascular wall.

31 bute to the maintenance and integrity of the vascular wall.

32 e development of eutrophic remodeling of the vascular wall.

33 neutrophils and monocytes/macrophages in the vascular wall.

34 nd fosters quiescence of the endothelium and vascular wall.

35 le (SS) red blood cell (RBC) adhesion to the vascular wall.

36 n of sphingolipid-dependent signaling in the vascular wall.

37 te KD, IgA plasma cells (PCs) infiltrate the vascular wall.

38 ily to the action of alpha-tocopherol in the vascular wall.

39 of regulation of platelet aggregation at the vascular wall.

40 ets function to protect the integrity of the vascular wall.

41 thylglutaryl-CoA reductase inhibitors on the vascular wall.

42 and and receptor expression in the allograft vascular wall.

43 t proinflammatory signal if activated on the vascular wall.

44 e on nitric oxide-dependent signaling in the vascular wall.

45 DL-derived cholesterol in macrophages in the vascular wall.

46 elative concentrations of TSP and vWF in the vascular wall.

47 ar inner border, and did not have a bounding vascular wall.

48 eometry and maintaining the integrity of the vascular wall.

49 ociated with perturbed matrix balance in the vascular wall.

50 ause of an inherent difficulty to access the vascular wall.

51 n sickle red blood cells and the endothelial vascular wall.

52 l of ADP-mediated signaling responses in the vascular wall.

53 he effects of platelets on components of the vascular wall.

54 ignificantly affecting the remodeling of the vascular wall.

55 and is highly expressed within the pulmonary vascular wall.

56 ivation and their capacity to infiltrate the vascular wall.

57 which are major producers of elastin in the vascular wall.

58 hich tumor cells tether, roll, and adhere to vascular walls.

59 age of vascular sprouts for stabilization of vascular walls.

60 extensive calcification in soft tissues and vascular walls.

61 ulated and localized in VSMCs in the injured vascular walls.

62 onocytes and MCP-1 specifically expressed in vascular walls.

63 eukocytes, and neutrophils accumulated along vascular walls.

64 lagen mRNA occurs in the pleura, airway, and vascular walls.

65 n vessels lumen by cells accumulation on the vascular walls.

66 Smooth muscle actin was only present in vascular walls.

67 that miRNAs are aberrantly expressed in the vascular walls after balloon injury.

68 , as well as interactions among cells of the vascular wall, all appear to influence vascular developm

69 n of matrix metalloproteinases (MMPs) in the vascular wall, allowing smooth muscle cells (SMCs) to di

70 y available imaging modalities can delineate vascular wall anatomy and, with novel probes, target bio

71 e (CX3CL1, FKN) is expressed in the inflamed vascular wall and absence of FKN reduces atherogenesis.

72 Cygb is expressed in the vascular wall and can consume NO in an O(2)-dependent ma

73 esting that endocannabinoid release from the vascular wall and CB(1)R activation reduces the vasocons

74 component of the glycocalyx involved in the vascular wall and endothelial glomerular permeability ba

75 titatively predict blood function in a given vascular wall and hemodynamic context.

76 derstanding of the complex interplay between vascular wall and immune system components.

77 s elevated, such as in the postnatal growing vascular wall and in vascular hypertrophic diseases.

78 are transported by Lp(a), and deposit in the vascular wall and induce local inflammation.

79 Elastin is a major protein component of the vascular wall and is responsible for its unusual elastic

80 145 is selectively expressed in VSMCs of the vascular wall and its expression is significantly downre

81 e protease whose activity may be involved in vascular wall and kidney homeostasis.

82 vealed high effectiveness in localization of vascular wall and lumen pathologies resulting from Takay

83 systems typically release drugs to both the vascular wall and non-target extravascular tissue.

84 process associated with inflammation of the vascular wall and perivascular space with cells of monoc

85 erations in the mechanical properties of the vascular wall and plays a crucial role in elastin loss d

86 of the dynamic nature of the atherosclerotic vascular wall and promises discovery and validation of t

87 scle cell (SMC) composes the majority of the vascular wall and retains phenotypic plasticity in respo

88 s in response to ischemia and hypoxia in the vascular wall and the kidney.

89 nes, altering the inflammatory milieu in the vascular wall and the kidney.

90 gonists may reduce leukocyte accumulation in vascular walls and contribute to their antiatherosclerot

91 miR-145 is the most abundant miRNA in normal vascular walls and in freshly isolated VSMCs; however, t

92 effectively the deposition of lipids in the vascular wall, and a combined dose showed a synergistic

93 e SMCs comprise the majority of cells in the vascular wall, and because IL-1 is implicated in atherog

94 hrough reduction of mechanical stress on the vascular wall, and directly by diminished stimulation fo

95 ular homeostasis, regulating the tone of the vascular wall, and its interaction with circulating bloo

96 tatin modulates beta-adrenergic signaling in vascular wall, and may have implications for cardiovascu

97 le cells, crosstalk between cells within the vascular wall, and recruitment of circulating progenitor

98 ed to adhere to the endothelial cells of the vascular wall, and the adhesion must be strong enough to

99 ence other cells, such as leukocytes and the vascular wall, and thus how they regulate hemostasis, va

100 e Ang II-induced AAA formation by inhibiting vascular wall apoptosis and extracellular matrix proteol

101 Cells within the vascular wall are coupled by gap junctions, allowing for

102 in the microenvironment organization within vascular walls are critical events in the pathogenesis o

103 ns (not true hemangiomas), except that their vascular walls are thinner owing to the constraints impo

104 and lymphocyte chemokine receptors (ChR) for vascular wall arrest and diapedesis.

105 stingly, defects in extracellular matrix and vascular wall assembly, were restricted to the aortic ar

106 ation of CTO is followed by a hibernation of vascular wall at distal coronary segments that fail to r

107 ther the biomechanical forces imposed on the vascular wall at this developmental stage act as a deter

108 New evidence on gender-based differences in vascular wall, atherosclerotic plaque deposition, pathop

109 However, a role for TSP-4 in vascular wall biology remains unknown.

110 Smooth muscle cells (SMC) of the vascular wall, bladder, myometrium, and gastrointestinal

111 mal stem cell (MSC)-like cells reside in the vascular wall, but their role in vascular regeneration a

112 and EETs prevented leukocyte adhesion to the vascular wall by a mechanism involving inhibition of tra

113 cle death and subsequent colonization of the vascular wall by proliferative adventitial cells that co

114 al alterations associated with aneurysms and vascular wall calcification.

115 a demonstrate that PBM interactions with the vascular wall can be reduced by autocrine production of

116 PDT results in complete vascular wall cell eradication with subsequent adventiti

117 Intrinsic vascular wall cells and lesional leukocytes alike can pr

118 that the trophic effect of catecholamines on vascular wall cells is dependent on a ROS-sensitive step

119 However, the direct effect of leptin on vascular wall cells is not fully understood.

120 ay between host inflammatory cells and donor vascular wall cells results in an intimal hyperplastic l

121 duce inflammatory cells and/or dysfunctional vascular wall cells to secrete growth factors that promo

122 rotein-B-containing lipoproteins, immune and vascular wall cells, and extracellular matrix.

123 lar inflammation by resident and nonresident vascular wall cells, but its role in the inflammatory pr

124 d to contribute to the aberrant phenotype of vascular wall cells, including fibroblasts, in pulmonary

125 As shown previously, human vascular wall cells, such as smooth muscle cells (SMC),

126 To determine the role of AT(1a) receptors on vascular wall cells, we developed AT(1a) receptor floxed

127 as activity in circulating hematopoietic and vascular wall cells, which are critical for maintaining

128 n association with impaired proliferation of vascular wall cells.

129 ribozyme in studying the effects of 12LO in vascular wall cells.

130 actor alpha did not augment stromelysin-3 in vascular wall cells.

131 ons induced by OxyHb might contribute to the vascular wall changes in the cerebral arteries following

132 umulate over time on plasma lipoproteins and vascular wall components and play an important role in t

133 Focal adhesions provide the vascular wall constituents with flexible and specific to

134 hat yields a three-dimensional view of these vascular wall constituents.

135 The vascular wall contains intimal endothelium and medial sm

136 ficant differences in the percentages of the vascular wall cross-sectional areas composed of intima (

137 es) and other markers of inflammation in the vascular wall (decreased production of monocyte chemoatt

138 These findings support the notion that vascular wall-derived Gas6 may play a pathophysiologic r

139 sels, which exhibited VSMC fragmentation and vascular wall disassembly.

140 pertrophic remodeling and may participate in vascular wall disease and remodeling.

141 ssible that insulin resistance itself in the vascular wall does not promote atherosclerosis.

142 on of permeability properties of the in situ vascular wall during exposure to toxin.

143 of Neo1 leukocytes to attach to endothelial vascular wall during inflammation.

144 chronic NEP-I on plasma cGMP concentrations, vascular wall ECE-1 activity, and ET-1 concentration, an

145 olves the production of nitric oxide (NO) by vascular wall endothelial cells and macrophages.

146 esses by promoting adhesion of leukocytes to vascular wall endothelium.

147 lates miR-204 and downregulates Sirt1 in the vascular wall/endothelium in vivo and in endothelial cel

148 re injury in apolipoprotein E-/- mice led to vascular wall expansion over a period of 4 weeks.

149 s found to reside in the lung mucosa and the vascular wall, express a wide variety of adhesion and co

150 The effect of multiple integrated stimuli on vascular wall expression of matrix metalloproteinases (M

151 can stably express a therapeutic gene in the vascular wall for > or =8 weeks, with minimal associated

152 s identify ILK as a key component regulating vascular wall formation by negatively modulating VSMC co

153 at the adventitia acts as a key regulator of vascular wall function and structure from the outside in

154 eases in intracellular Ca2+ ([Ca2+]i) in the vascular wall (fura 2 fluorescence) and phosphorylation

155 nephrine (NE) directly contributes to normal vascular wall growth and worsening of hypertrophy, ather

156 y venules were dilated, and up to 70% of the vascular wall had no smooth muscle cells.

157 Thrombospondin-1 (TSP-1) expression in the vascular wall has been related to the development of ath

158 This regulates NO levels in the vascular wall; however, the underlying molecular basis o

159 d that peroxidation products produced in the vascular wall (ie, 4-hydroxynonenal) upregulate adiponec

160 lowing endothelial injury through effects on vascular wall IGF-1R.

161 In addition to vascular wall imaging, this detector may also be used as

162 motility, and adhered strongly to the renal vascular wall in a chemokine receptor CX3CR1-dependent m

163 rvation that IgA plasma cells infiltrate the vascular wall in acute KD.

164 -1 is present and functionally active in the vascular wall in atherosclerosis.

165 EP, the ectoenzyme that degrades BNP, in the vascular wall in atherosclerosis.

166 Leukocytes normally marginate toward the vascular wall in large vessels and within the microvascu

167 h-induced contractile differentiation in the vascular wall in part via miR-145-dependent regulation o

168 ediator in the remodeling that occurs in the vascular wall in response to injury.

169 uctural and functional reorganization of the vascular wall in response to the new local biomechanical

170 erial shear stress (2000(-s)) and to injured vascular wall in vivo after carotid ligation.

171 The recruitment of cells to the vascular wall in vivo or the capture of cell subpopulati

172 educed melanoma cell adhesion to the injured vascular wall in vivo.

173 dent in smooth muscle cells of bronchial and vascular walls, in alveolar macrophages, and some vascul

174 ve oxygen species (ROS)-producing systems in vascular wall include NADPH (reduced form of nicotinamid

175 CM proteins comprise different layers of the vascular wall including collagen types I, III, and IV, a

176 adhere avidly to multiple components of the vascular wall, including laminin.

177 to the endothelium but occur throughout the vascular wall, including smooth muscle cells.

178 A "vascular wall infection" hypothesis, responsible for end

179 orta and that these proteases act to amplify vascular wall inflammation that leads to AAAs.

180 ctivated, failed to support initial steps of vascular wall inflammation.

181 e in conditions such as cardiac hypertrophy, vascular wall injury, cardiac surgery, ischemic precondi

182 Thus, LRP1 has a pivotal role in protecting vascular wall integrity and preventing atherosclerosis b

183 rgeting MMP-3 may be effective in protecting vascular wall integrity.

184 ion, prevent vSMC reprogramming, and promote vascular wall integrity.

185 ronic inflammatory response initiated at the vascular wall, interactions of P. gingivalis with endoth

186 ently coupled or co-administered) across the vascular wall into tumor tissue.

187 e utility of preoperative imaging to predict vascular wall invasion, which carries adverse prognostic

188 Leukocyte adhesion to the vascular wall is a critical early step in the pathogenes

189 interaction of circulating cells within the vascular wall is a critical event in chronic inflammator

190 reactive oxygen species (ROS) throughout the vascular wall is a feature of cardiovascular disease sta

191 The accumulation of macrophages in the vascular wall is a hallmark of atherosclerosis.

192 ed metabolism of cells forming the pulmonary vascular wall is a key currently irreversible pathologic

193 We concluded that breaching of the vascular wall is a rate-limiting step for intravasation,

194 Stretch of the vascular wall is an important stimulus to maintain smoot

195 Mechanical strain in the vascular wall is anisotropic and mainly in the circumfer

196 e recent observations demonstrating that the vascular wall is comprised of phenotypically heterogeneo

197 f macrophages and smooth muscle cells in the vascular wall is critical for the development of atheros

198 Remodeling of the injured vascular wall is dependent on the action of several extr

199 expression and function of connexins in the vascular wall is important during atherosclerosis.

200 grees C, indicating that NO diffusion in the vascular wall is no longer free, but markedly dependent

201 ual Nox homologues in specific layers of the vascular wall is unclear.

202 n of activated T lymphocytes observed within vascular wall lesions during atherogenesis.

203 Vascular wall levels of soluble beta-amyloid1-40 (Abeta1

204 cells by VSMCs did not induce the release of vascular wall matrix proteases but was associated with a

205 d to test the hypothesis that PDT alters the vascular wall matrix thereby inhibiting invasive cell mi

206 ults imply that the NO diffusion rate in the vascular wall may be upregulated and downregulated by ce

207 In this study, a vascular wall mechanics model is used to predict the rel

208 he focus of this review is on changes in the vascular wall mediated by this receptor and primarily re

209 d evidence that endothelial shear stress and vascular wall morphology along the course of human coron

210 g to a reduction of mechanical resistance of vascular wall, most commonly caused by its defected stru

211 ts of VEGF on another major cell type in the vascular wall, namely, the vascular smooth muscle cell (

212 the recruitment of inflammatory cells in the vascular wall, necessary processes for the progression o

213 proliferation, migration, and injury-induced vascular wall neointima formation.

214 retention and modification of lipids in the vascular wall, NKT cells may be involved in promoting th

215 ed decrease in AT2 is a direct effect on the vascular wall, not requiring systemic responses, and tha

216 he hypothesis that apoptosis of cells in the vascular wall of coronary arteries can be detected on SP

217 attachment of circulating tumor cells to the vascular wall of distant tissues.

218 expression was significantly reduced in the vascular wall of Gas6(-/-) mice compared with WT.

219 ribed sites of hematopoietic activity in the vascular wall of mid-gestation vertebrate embryos, and p

220 le smooth muscle cell differentiation in the vascular wall of the ductus arteriosus and adjacent desc

221 ies; this suggests that focal defects in the vascular wall or blood flow must be associated with a hy

222 new evidence on gender-based differences in vascular wall or metabolic alterations, atherosclerotic

223 maturation and die by E12.5, with increased vascular wall p53 activity.

224 The vascular wall participates in the pathogenesis of sickle

225 he notion that the adventitia is integral to vascular wall pathogenesis, and raising potential implic

226 statins may specifically preempt disordered vascular wall pathology and constitute physiological evi

227 tions of blood cells and components with the vascular wall perpetuate both thrombotic and inflammator

228 s (SMCs), one of the major cell types of the vascular wall, play a critical role in the process of an

229 s, we hypothesize that Gas6 derived from the vascular wall plays a role in venous thrombus formation.

230 terol and direct atherogenic actions through vascular wall processes such as monocyte recruitment and

231 urrent body of evidence for the existence of vascular wall progenitor cell subpopulations from develo

232 ta indicate the involvement of some of these vascular wall progenitor cells in vascular disease state

233 ke characteristics that support and regulate vascular wall progenitor cells.

234 s, in which the retention of lipoproteins by vascular wall proteoglycans is critical.

235 Diseases of ectopic calcification of the vascular wall range from lethal orphan diseases such as

236 h both 11betaHSD isozymes are present in the vascular wall, reactivation of glucocorticoids by 11beta

237 ntion and accumulation of macrophages in the vascular wall remain unclear.

238 5-LOX1-15(S)-HETE axis plays a major role in vascular wall remodeling after balloon angioplasty.

239 ated PAK1 activation plays a crucial role in vascular wall remodeling and it could be a potential tar

240 of NFATs by VIVIT on balloon injury-induced vascular wall remodeling events, including smooth muscle

241 NFATc1-cyclin D1/CDK6 activity in mediating vascular wall remodeling following injury.

242 This review focuses on the mechanisms of vascular wall remodeling in TV, including the intimal ac

243 /STAT-3 signaling plays an important role in vascular wall remodeling particularly in the settings of

244 s suggest that PKN1 plays a critical role in vascular wall remodeling, and therefore, it could be a p

245 Toward understanding the mechanisms of vascular wall remodeling, here we have studied the role

246 s, matrix-degrading protease expression, and vascular wall remodeling, important hallmarks of arteria

247 role of human 15-lipoxygenase 1 (15-LOX1) in vascular wall remodeling, we have studied the effect of

248 -STAT3-dependent MCP-1 expression leading to vascular wall remodeling.

249 HASMC proliferation and migration as well as vascular wall remodeling.

250 naling axis is involved in the modulation of vascular wall remodeling.

251 on for vascular repair during injury-induced vascular wall remodeling.

252 onocyte chemotactic protein 1 (MCP1)-induced vascular wall remodeling.

253 cular smooth muscle cell (VSMC) migration in vascular wall remodeling.

254 h, as we reported previously, is involved in vascular wall remodeling.

255 xtracellular matrix (ECM) is associated with vascular wall remodelling and impaired reactivity, a pro

256 Ca(2+) signalling promotes vascular wall remodelling by regulating cell proliferati

257 ocess that contributes to pathophysiological vascular wall remodelling.

258 : 1) to investigate the relationship between vascular wall shear stress and flow-mediated dilation (F

259 es, as well as disruption of redox-dependent vascular wall signaling processes.

260 ell differentiation and stabilization of the vascular wall significantly contribute to the response t

261 whereas cystatin C is normally expressed in vascular wall smooth muscle cells (SMCs), this cysteine

262 Fbeta to regulate mural cell development and vascular wall stability.

263 Vascular wall stretch is the major stimulus for the myog

264 steine is multifactorial, affecting both the vascular wall structure and the blood coagulation system

265 his respect, therefore, platelet adhesion to vascular wall structures, to one another (aggregation),

266 rs even without the presence of virus in the vascular wall, suggesting that inflammatory and immune r

267 vented HCD-induced lipid accumulation in the vascular wall, suggesting that the antibody itself may h

268 he direct effects of statin treatment on the vascular wall, supporting the notion that this effect is

269 ochetes from heart base and synovium but not vascular walls, tendons, or ligaments.

270 functional significance relative to that of vascular wall TF is poorly defined.

271 ins are novel signaling receptors within the vascular wall that affect vasomotor tone, and may play a

272 y process of lipid-rich lesion growth in the vascular wall that can cause life-threatening myocardial

273 that regulate macrophage recruitment to the vascular wall, the ability of growth factors to regulate

274 in patients with ischemic versus those with vascular wall thickening was statistically significant (

275 formation, including lumen configuration and vascular wall thickness, and physiologic data, such as m

276 exert their anti-inflammatory effects on the vascular wall through a variety of molecular pathways of

277 , we observed intrinsic abnormalities in the vascular walls throughout the cutaneous vasculature.

278 -like domains and shows marked expression in vascular wall tissue.

279 mechanisms of this adaptive response of the vascular wall to changes in its biomechanical environmen

280 also act individually as gatekeepers of the vascular wall to help preserve vascular integrity while

281 The response of the arterial vascular wall to injury is characterized by vascular smo

282 red by the endothelium and migrate along the vascular wall to permissive sites of transmigration.

283 (VWF) initiates platelet adhesion to injured vascular wall to stop bleeding.

284 677C>T as a model of chronic exposure of the vascular wall to varying 5-MTHF levels in 218 patients u

285 Rather, it moved progressively across the vascular wall toward the luminal surface.

286 The interaction between leukocytes and vascular wall via overexpression of various molecules fa

287 er vasculature, which remain anchored to the vascular wall via von Willebrand factor and reveal signi

288 alyl-Lewis-x), and then firmly adhere to the vascular wall (via interactions between integrins and IC

289 Bacterial presence at the vascular wall was observed specifically in areas of vasc

290 ion of cellular growth in the myocardium and vascular wall, was investigated.

291 cholesterol deposition and oxidation in the vascular wall, which also exhibited increased adhesion o

292 s a hydrostatic pressure gradient across the vascular wall, which leads to a deeper penetration of mo

293 ffects of lipid lowering at the level of the vascular wall, which may influence the biology of the at

294 To the extent that chronic infection of the vascular wall with CMV contributes to atherogenesis, the

295 es via blockade of aldosterone action in the vascular wall with MR antagonists (i.e., spironolactone,

296 the interaction of tissue factor (TF) in the vascular wall with platelets and coagulation factors in

297 tumours is thought to result from malformed vascular walls with leaky cell-to-cell junctions.

298 ntly increased in proliferative VSMCs and in vascular walls with neointimal growth.

299 ession is significantly downregulated in the vascular walls with neointimal lesion formation and in c

300 as important in mediating HDL binding to the vascular wall, with a 48+/-16% increase in accumulation