ライフサイエンスコーパス: vascular wall

1 e codistribution of LOXL2 and elastin in the vascular wall.

2 and is highly expressed within the pulmonary vascular wall.

3 ivation and their capacity to infiltrate the vascular wall.

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

5 ies compromise interactions with the damaged vascular wall.

6 an antiatherogenic lipid environment in the vascular wall.

7 drive atherosclerosis by accumulating in the vascular wall.

8 ing monocytes to the injured atherosclerotic vascular wall.

9 cholesterol-accumulating macrophages in the vascular wall.

10 ateral induction throughout the width of the vascular wall.

11 ively regulating monocyte recruitment to the vascular wall.

12 elium, inhibiting their migration across the vascular wall.

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

14 mulation of fluorescent myeloid cells in the vascular wall.

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

16 zed as an inflammatory disease involving the vascular wall.

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

18 composition and the different layers of the vascular wall.

19 Th1 subset and recruits macrophages into the vascular wall.

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

21 drenergic modulation of eNOS pathways in the vascular wall.

22 ng vascular development and within the adult vascular wall.

23 is essential to maintain homeostasis of the vascular wall.

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

25 lial cells and guiding leukocytes across the vascular wall.

26 nflammatory and proliferative changes in the vascular wall.

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

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

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

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

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

32 events inappropriate apoptotic damage to the vascular wall.

33 the pathogenesis of several disorders of the vascular wall.

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

35 results from passive lipid deposition in the vascular wall.

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

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

38 e development of eutrophic remodeling of the vascular wall.

39 neutrophils and monocytes/macrophages in the vascular wall.

40 nd fosters quiescence of the endothelium and vascular wall.

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

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

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

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

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

46 thylglutaryl-CoA reductase inhibitors on the vascular wall.

47 ion and fibroproliferative remodeling in the vascular wall.

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

49 of regulation of platelet aggregation at the vascular wall.

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

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

52 eometry and maintaining the integrity of the vascular wall.

53 ociated with perturbed matrix balance in the vascular wall.

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

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

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

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

58 ignificantly affecting the remodeling of the vascular wall.

59 Smooth muscle actin was only present in vascular walls.

60 age of vascular sprouts for stabilization of vascular walls.

61 extensive calcification in soft tissues and vascular walls.

62 is factor alpha (TNF-alpha), particularly in vascular walls.

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

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

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

66 eukocytes, and neutrophils accumulated along vascular walls.

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

68 ce binding with von Willebrand factor on the vascular walls.

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

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

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

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

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

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

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

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

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

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

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

80 ose that the interaction between the uterine vascular wall and its adjacent adipose tissue may provid

81 145 is selectively expressed in VSMCs of the vascular wall and its expression is significantly downre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 Cells in vascular walls are exposed to blood pressure variability

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

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

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

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

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

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

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

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

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

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

115 al alterations associated with aneurysms and vascular wall calcification.

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

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

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

126 n association with impaired proliferation of vascular wall cells.

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

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

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

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

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

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

133 The vascular wall contains intimal endothelium and medial sm

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

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

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

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

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

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

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

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

142 optosis, thereby promoting resilience of the vascular wall during oxidative stress.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 -1 is present and functionally active in the vascular wall in atherosclerosis.

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

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

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

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

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

168 characterize the cellular morphology of the vascular wall in unmanipulated vessels and during retrac

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 Fibronectin in the vascular wall promotes inflammatory activation of the en

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

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

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

231 power, although chronic assessment revealed vascular wall recovery in lesions without steam pop.

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

233 5-LOX1-15(S)-HETE axis plays a major role in vascular wall remodeling after balloon angioplasty.

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

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

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

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

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

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

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

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

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

243 a novel way to regulate brain entry through vascular wall remodeling.

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

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

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

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

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

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

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

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

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

253 ocess that contributes to pathophysiological vascular wall remodelling.

254 tions in collagen III, which predominates in vascular walls, result in vascular Ehlers-Danlos syndrom

255 n-recognition receptors TLR7 and TLR9 in the vascular wall, resulting in profound vascular dysfunctio

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

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

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

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

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

261 Vascular wall stretch is the major stimulus for the myog

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

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

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

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

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

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

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

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

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

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

272 This was associated with reduced pulmonary vascular wall thickness, increased lung levels of ANP (a

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

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

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

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

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

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

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

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

281 677C>T as a model of chronic exposure of the vascular wall to varying 5-MTHF levels in 218 patients u

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

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

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

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

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

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

288 l and regressed conditions, cells within the vascular wall were planar polarized, with an integrin- a

289 nt macrophages and leukocyte adhesion to the vascular wall were significantly decreased in empagliflo

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

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

292 porting these pro-inflammatory events in the vascular wall, which may contribute to the increased ass

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