ライフサイエンスコーパス: mural

1 and morphologic characteristics (polypoid or mural).

2 tively evaluate the degree of flaking of the murals.

3 enhance our understanding of YKL-40 in both mural and endothelial cell biology.

4 pathological angiogenesis, such as vascular mural and endothelial cells, macrophages, choroidal fibr

5 ng techniques clearly highlight endoluminal, mural and extramural enteric details and provide vascula

6 We observed that mural and mesenchymal cell markers, including pdgfrbeta,

7 ic stability were evaluated in rat models of mural and occlusive carotid artery thrombosis.

8 early blastocysts, MOEP19 localized in both mural and polar trophectoderm and a subset of embryos sh

9 ytes of the AVC contributed to the tricuspid mural and posterior leaflets, the mitral septal leaflet,

10 d that improve visualization of the mucosal, mural, and perienteric inflammation associated with infl

11 iautomated software could accurately measure mural attenuation and thickness, the selected terminal i

12 Quantitative measures of mural attenuation and wall thickness at CT enterography

13 Quantitative measures of terminal ileal mural attenuation and wall thickness correlated signific

14 d measurements at each location) to quantify mural attenuation and wall thickness.

15 Quantitative measures of mural attenuation are sensitive markers of small bowel i

16 Mural attenuation for different bowel loops was compared

17 Mural attenuation was measured in the distended and coll

18 Visual enhancement and quantitative mural attenuation were significantly correlated (P < .00

19 nd demonstrate that microglia respond to the mural basement membrane in an isoform-specific manner.

20 signaling are modulated by components of the mural basement membrane.

21 tissue MVD is actually inversely related to mural blood flow.

22 0-V5-His were localized to vessel walls in a mural cell (pericyte) position indicating a possible dir

23 of carcinoma cells and in vessel walls in a mural cell (pericyte) position.

24 ney is dependent on the kinetics of vascular mural cell (VMC) differentiation.

25 We now demonstrate that mural cell accumulation evident at embryonic day (E) 13.

26 nsity, and normalized vessels with increased mural cell attachment.

27 that the Arf tumor suppressor gene regulates mural cell biology in the hyaloid vascular system (HVS)

28 g glomerular capillary development, arterial mural cell coating, and lymphatic vessel development, re

29 These progenitors reside in the mural cell compartment of the adipose vasculature, but n

30 e (NOS) inhibitor, we found that NO mediates mural cell coverage as well as vessel branching and long

31 use of impaired lymphatic drainage, aberrant mural cell coverage fostered the accumulation of fibroge

32 is both necessary and sufficient to support mural cell coverage in arteries using genetic rescue in

33 ll migration, which likely led to stabilized mural cell coverage of mature vessels.

34 NEM inoculation specifically promoted mural cell coverage of tumor vessels and decreased vascu

35 demonstrated RhoA activation induced loss of mural cell coverage on the endothelium and reduced endot

36 lts in severe mucosal hemorrhage, incomplete mural cell coverage on vessel walls, and gastrointestina

37 phatic vessels with reduced and disorganized mural cell coverage.

38 1) with a Cre-loxP approach in mice leads to mural cell defects and postnatal lethality.

39 brain tissues display a marked reduction in mural cell density as well as abnormal vessel wall morph

40 ons synergistically with TGFbeta to regulate mural cell development and vascular wall stability.

41 demonstrate embryonic hemorrhaging, altered mural cell development, or lethality.

42 To explore the cues that regulate mural cell differentiation and homeostasis, we have gene

43 Our findings emphasize that the level of mural cell differentiation and stabilization of the vasc

44 l cells, Cx43-/- progenitors did not undergo mural cell differentiation as did Cx43+/+ cells.

45 ells did produce latent TGF-beta and undergo mural cell differentiation in response to exogenous TGF-

46 own a role for TGF-beta in coculture-induced mural cell differentiation, growth inhibition resulting

47 OTCH3 is necessary for endothelial-dependent mural cell differentiation, whereas overexpression of NO

48 helial cells and undergo endothelial-induced mural cell differentiation.

49 f later stages of vessel assembly, including mural cell differentiation.

50 mediates TGF-beta activation and subsequent mural cell differentiation.

51 ication is necessary for endothelial-induced mural cell differentiation.

52 PDGFRbeta-dependent signal transduction and mural cell function.

53 model revealed that NO mediates endothelial-mural cell interaction prior to vessel perfusion and als

54 athway causes disruption of endothelial cell-mural cell interactions and loss of mural cells.

55 also a key mediator of endothelial-vascular mural cell interactions, a role that may contribute to t

56 ll remodelling in association with losses in mural cell investment and disruptions in arterial-venous

57 Angiogenesis, mural cell investment, leukocyte recruitment, vascular p

58 Moreover, Notch3 deletion impairs mural cell investment, resulting in progressive loss of

59 ation of an agonist Notch3 antibody prevents mural cell loss and modifies plasma proteins associated

60 ndothelial precursor cell marker (CD133) and mural cell markers (calponin, desmin, and smooth muscle

61 ndent enlargement, ii) altered expression of mural cell markers (eg, down-regulation of NG2 and up-re

62 od-perfused vascular channels that coexpress mural cell markers smooth muscle alpha-actin and platele

63 proliferation, expression of mesenchymal and mural cell markers, and coronary blood vessel formation.

64 Impaired mural cell migration, differentiation, partial embryonic

65 ARCL1 secretion from quiescent ECs inhibited mural cell migration, which likely led to stabilized mur

66 epatocyte growth factor (HGF), a mediator of mural cell motility, was up-regulated by Ang1 stimulatio

67 alphaSMA), and iii) dramatic alterations in mural cell phenotype near the optic nerve head.

68 n of mesodermal progenitor cells to a mature mural cell phenotype through activation of the transform

69 atrix adhesion is a major determinant of the mural cell phenotype.

70 -derived NO induces directional migration of mural cell precursors toward endothelial cells.

71 irect the recruitment and differentiation of mural cell precursors.

72 To further dissect the role of NO in mural cell recruitment and vascular morphogenesis, we pe

73 ate that endothelial cell-derived NO induces mural cell recruitment as well as subsequent morphogenes

74 In the developing vasculature, mural cell recruitment is associated with the functional

75 derived growth factor B (PDGF-B), leading to mural cell recruitment thereby contributing to vascular

76 promoting arteriogenesis, angiogenesis, and mural cell recruitment to immature angiogenic sprouts.

77 Our results implicate aberrant mural cell recruitment to lymphatic vessels in the patho

78 Inhibition of mural cell recruitment to the dorsal aorta through disru

79 Mural cell recruitment to the growing endothelial tube i

80 gnaling pathways, which are both crucial for mural cell recruitment, via its intracellular domain.

81 tients with glioblastomas developed vigorous mural cell-associated vascular channels but few endothel

82 d GSDCs gave rise to tumors harboring robust mural cell-associated vascular channels.

83 deficient mice and led to a higher number of mural cell-invested vessels than control transfection.

84 man bone marrow stromal cells, which adopt a mural cell-like phenotype that recapitulates barrier fun

85 Defective mural-cell coverage is associated with the poorly organi

86 found a higher number and magnitude of NG2+ mural-cell mediated capillary constrictions in the hippo

87 nt investment of the vascular endothelium by mural cells (i.e., pericytes and vascular smooth muscle

88 Mural cells (MCs) consisting of vascular smooth muscle c

89 (CMs), endothelial cells (ECs), and vascular mural cells (MCs) differentiated from hiPSCs.

90 uration and stability require recruitment of mural cells (MCs) to the nascent vessel.

91 Recruitment of mural cells (MCs), namely pericytes and smooth muscle ce

92 Mural cells (pericytes and vascular smooth muscle cells)

93 by loss of alpha5 from Pdgfrb-Cre expressing mural cells (pericytes and vascular smooth muscle cells)

94 s may be related to the presence of vascular mural cells (pericytes or smooth muscle cells).

95 Mesenchymal cells including microvascular mural cells (pericytes) are major progenitors of scar-fo

96 ed here are the myofibroblasts, fibroblasts, mural cells (pericytes) of the vasculature, bone marrow-

97 BM-derived periendothelial vascular mural cells (pericytes) were detected at sites of neovas

98 otypic interactions of endothelial cells and mural cells (smooth muscle cells or pericytes) are cruci

99 Endothelial cells and mural cells (smooth muscle cells, pericytes, or fibrobla

100 Mural cells (vascular smooth muscle cells and pericytes)

101 othelial trafficking with pericytes/vascular mural cells (VMC), an interaction crucial to vessel stab

102 Mural cells actively participated during the whole angio

103 ressed tip cell migration and recruitment of mural cells and adventitial macrophages.

104 capillaries composed of endothelium lacking mural cells and altered sub-endothelial extracellular ma

105 te chemoattractant protein-1 (MCP-1) in cyst mural cells and increased excretion of this chemokine in

106 at Notch3 is important for the investment of mural cells and is a critical regulator of developmental

107 dhesive interactions between endothelial and mural cells and its impact on vascular barrier function

108 signaling axis disrupted the association of mural cells and lymphatic vessels, improved lymphatic dr

109 he stabilization of nascent blood vessels by mural cells and may be exploited to control angiogenesis

110 that suggested based on lineage tracing that mural cells are adipogenic, contrasting with the conclus

111 Mural cells are also recruited by endothelial cells to f

112 Mural cells are emerging as multipotent progenitors of p

113 g to show that caSMCs derive from pericytes, mural cells associated with microvessels, and that these

114 ated GFP(+) cells were further identified as mural cells based on the presence of the specific XLacZ4

115 gene whose expression is robustly induced in mural cells by coculturing with endothelial cells.

116 DGFR-beta is also involved in recruitment of mural cells by neovessels, regulating maturation of the

117 ontributes to the proangiogenic abilities of mural cells cocultured with endothelial cells.

118 ent required for survival of endothelial and mural cells during vascularization.

119 Pericytes are vascular mural cells embedded in the basement membrane of blood m

120 Pericytes are vascular mural cells embedded within the basal lamina of blood mi

121 stead, we identify a stromal source of SLIT, mural cells encircling blood vessels, and show that loss

122 hrough VEGFA-laden microparticles and act as mural cells for newly formed vessels, driving scar progr

123 , we observed a rapid physical withdrawal of mural cells from the endothelium that was accompanied by

124 t in vivo evidence for a functional role for mural cells in patterning and stabilization of the early

125 bility of a broad range of investigations of mural cells in vascular development, neurovascular coupl

126 increased the proliferation and migration of mural cells in vitro and improved perivascular cell cove

127 ecise tracing of the lineage contribution of mural cells in vivo than previous versions.

128 The number of endothelial and mural cells increased significantly, and the local tissu

129 xamined the emergence and functional role of mural cells investing the dorsal aorta during early deve

130 nication between endothelial cells (ECs) and mural cells is critical in vascular maturation.

131 RISPR-mediated knockout of N-cadherin in the mural cells led to loss of barrier function, and overexp

132 ed cardiomyocytes, endothelial, and vascular mural cells matured in vitro for 14 days.

133 defects with lack of proper investment with mural cells of both large and small vessels.

134 Pericytes are perivascular mural cells of brain capillaries.

135 the potential targets is the pericytes, the mural cells of microvessels, which regulate microvascula

136 l cells of Wnt7b/canonical Wnt signaling are mural cells of periureteric bud capillaries in the nasce

137 further showed that N-cadherin expression in mural cells plays a key role in barrier function, as CRI

138 ells to areas of hypoxia, where perivascular mural cells present stromal-derived factor 1 (CXCL-12) a

139 Here we report that mural cells require ephrin-B2, a ligand for Eph receptor

140 However, the mechanistic details of how mural cells stabilize vessels are not fully understood.

141 ctivity and increase in RhoA activity in the mural cells themselves upon inflammation.

142 othelial cells induce the differentiation of mural cells through activation and induction of NOTCH3.

143 el perfusion and also induces recruitment of mural cells to angiogenic vessels, vessel branching, and

144 r maturation characterized by the failure of mural cells to migrate around endothelial cells.

145 s integrin-ligand pair block the adhesion of mural cells to proliferating endothelia in vitro and in

146 asculature relies on active participation of mural cells to stabilize endothelium and a basal level o

147 strains, only those that marked perivascular mural cells tracked the cold-induced beige lineage.

148 nitors and induce their differentiation into mural cells via contact-dependent transforming growth fa

149 that capillary pericytes are a population of mural cells with distinct morphological, molecular and f

150 mechanistic insights into the cooperation of mural cells with endothelial cells induced by YKL-40 dur

151 pericytes and vascular smooth muscle cells (mural cells) ensures the formation of a mature and stabl

152 Furthermore, in mural cells, a dominant-negative Mastermind-like1 constr

153 b enhanced the proliferation of Wnt7b target mural cells, an effect that associated with decreased ex

154 e supported by the fibroblasts, which act as mural cells, and their growth is increased by the presen

155 sis or angiogenesis, requires recruitment of mural cells, generation of an extracellular matrix and s

156 th muscle cell-specific alpha-actin-positive mural cells, indicative of maturation.

157 s by which nascent vessels are invested with mural cells, is important in angiogenesis.

158 mediates coating of developing vessels with mural cells, leading to the formation of a mature vascul

159 indicated that Notch3, which is expressed in mural cells, mediates these cell-cell interactions.

160 hich line the vascular lumen, and associated mural cells, namely vascular smooth muscle cells and per

161 o suppress cell proliferation and to recruit mural cells, thereby establishing endothelial quiescence

162 eural crest migration and the recruitment of mural cells, which are essential for vascular stability.

163 atial coordination of endothelial cells with mural cells, which delivers oxygen and nutrients.

164 Loss of mural cells, which encompass pericytes and vascular smoo

165 n macrophages and endothelial cells, but not mural cells.

166 h factor receptor (PDGFR)-beta in associated mural cells.

167 rocytes, fibroblasts, endothelial cells, and mural cells.

168 te its own expression and that of JAGGED1 in mural cells.

169 itors of endothelial cells, blood cells, and mural cells.

170 endothelial cells as well as of perivascular mural cells.

171 nflammatory and mitogenic status of resident mural cells.

172 ial cell-mural cell interactions and loss of mural cells.

173 expressed by proliferating but not quiescent mural cells.

174 N-cadherin-dependent cell-cell adhesion with mural cells.

175 ial for interactions between endothelial and mural cells.

176 sion were larger and more densely covered by mural cells.

177 in these mice, with abnormal recruitment of mural cells.

178 vascular network concentrically wrapped with mural cells.

179 ly expressing a diphtheria toxin receptor in mural cells.

180 in the retinal venous system and associated mural cells.

181 is and in the recruitment and maintenance of mural cells.

182 he outer vessel layer and differentiate into mural cells.

183 formations involving impaired recruitment of mural cells.

184 In 16 subjects mural changes were not found.

185 Acquisition of a mural coat and maturation of the vasculature promotes re

186 rosis that lymphatic vessels exhibit ectopic mural coverage and that this occurs early during the dis

187 nt rats but was displayed in most tubule and mural cyst cell nuclei of androgen-replete rats.

188 Synthesis by mural cyst epithelial cells or an exogenous source are t

189 eak, collections of extruded fecal material, mural defect, wall thickening, abnormal enhancement, fre

190 egree of distention and the visualization of mural detail were qualitatively scored on a five-point s

191 Intra-mural echogenic dots were seen in one neonate in the stu

192 These results show that when confounding mural effects are minimized, lipid deposition is promote

193 mmation of a segment of bowel by quantifying mural enhancement in patients examined with CT enterogra

194 At multi-detector row CT, peak mural enhancement of the normal small bowel occurs on av

195 ic phase (which represented peak small-bowel mural enhancement), and the venous phase.

196 l homogeneity, lack of internal enhancement, mural enhancement, and characteristic location.

197 erum, and cyst fluid and MCP-1 production by mural epithelial cells cultured from the cysts of human

198 Mural epithelial cells from ADPKD cysts and normal human

199 +/+ by -89.4%, and AR expression within cyst mural epithelial cells was strikingly decreased.

200 by adenosine cAMP, which is produced within mural epithelial cells.

201 source of some of this chemokine may be the mural epithelium of cysts.

202 trated significantly better visualization of mural features in the duodenum (P = .003), jejunum (P =

203 nt distention and excellent visualization of mural features in the gastrointestinal tract.

204 ) and a trend toward better visualization of mural features in the stomach (P = .092).

205 lesion consisted of a polypoid, left atrial, mural fibrin thrombus with anaplastic tumor cells lining

206 rease in steady-state levels of KL-1 mRNA in mural granulosa but not cumulus cells.

207 Pro-ADAMTS-1 of 110 kDa was identified in mural granulosa cells and appears localized to cytoplasm

208 re highly expressed in cumulus cells than in mural granulosa cells of mouse antral follicles.

209 w in the cumulus and virtually absent in the mural granulosa cells of preovulatory follicles.

210 zing hormone (LH) activates receptors in the mural granulosa cells of the ovarian follicle.

211 of progesterone receptor, genes expressed in mural granulosa cells that regulate the expression of no

212 tes reduced KL-2 but not KL-1 mRNA levels in mural granulosa cells treated with testosterone plus FSH

213 Cervical artery dissection (CeAD), a mural hematoma in a carotid or vertebral artery, is a ma

214 Certain MR imaging-derived mural hemodynamic parameters correlate with disease chro

215 Mural hyperenhancement and increased mural thickness are

216 k has been performed to preserve the ancient murals in the Mogao Grottoes by Dunhuang Cultural Resear

217 be administered i.v. to the animal to detect mural inflammation or tumor vascularity.

218 easibility of targeted left ventricular (LV) mural injection using real-time MRI (rtMRI).

219 d lineage-restricted progenitor cells in the mural layers of postnatal blood vessels, possessing high

220 seen in the same leaflets, ie, the tricuspid mural leaflet and mitral septal leaflet were longer, the

221 Two children (25%) with mural lesions and 1 (4%) with a choroidal lesion suffere

222 Xenotransplantation of tumor-derived mural-like cells (GSDCs) expressing YKL-40 in mice devel

223 on between endothelial cells and mesenchymal mural-like cells for tumor angiogenesis.

224 This study establishes mural-like tumor cells differentiated from GSCs as a sig

225 cular channels of VM in GBM were composed of mural-like tumor cells that strongly express VEGF recept

226 ouse strains that mark adipocyte, muscle and mural lineages, three proposed beige origins.

227 P=0.41) but did strongly correlate with both mural macrophage density (r=0.79, P=0.007) and neovessel

228 m and manifest as an intraluminal polyp or a mural mass.

229 ntraluminal polypoid masses and 13 (39%) had mural masses; in three patients (9%), the tumor was not

230 A typically thin mural myofibroblastic cuff was smooth muscle actin posit

231 limit the amount of interstitium from which mural myofibroblasts can be recruited.

232 al imaging included multiloculation (56.9%), mural nodularity (16.5%), and biliary ductal dilatation

233 Multivariate analysis demonstrated mural nodularity and atypical cytopathology were predict

234 main-duct IPMN and for branch-duct IPMN with mural nodularity or positive cytology irrespective of lo

235 n, distribution, size, number, cytology, and mural nodularity were correlated with IPMN pathology.

236 e, size, location, septation, calcification, mural nodularity, pancreatic duct involvement, and prese

237 m, dilated main pancreatic duct (MPD) >6 mm, mural nodule (MN) and "positive" cytology as high risk s

238 eatic duct dilatation, a solid component, or mural nodule) require further evaluation with advanced i

239 eck location, larger MCN, solid component or mural nodule, and duct dilation.

240 Mural nodules can be detected and sampled effectively by

241 The presence of mural nodules was associated with malignant and invasive

242 evaluated images for lesion location, septa, mural nodules, communication with MPD, extent and diamet

243 Presence of mural nodules, dilated MPD (>10-mm diameter), or thick s

244 or IPMN features such as age, cyst location, mural nodules, serum tumor markers, or bilirubin.

245 gard to the size of the lesions, presence of mural nodules, thickening of the wall, dilation of the m

246 t IPMNs were less than 3 cm in size, without mural nodules, thickening of the wall, or other features

247 was present: MPD diameter larger than 10 mm, mural nodules, vascular encasement, peripancreatic lymph

248 gnancy in tumors <30 mm, without symptoms or mural nodules.

249 excludes prognostic subgroups stratified for mural penetration (T1-4) or nodal involvement (N1 vs. N2

250 ion and enlargement require proliferation of mural renal epithelial cells and the transepithelial sec

251 ltiple roles that pericytes (also defined as mural, Rouget, or perivascular cells) may play during an

252 iant cell transformation, and central venous mural sclerosis.

253 ppendiceal diameter, wall thickness, loss of mural stratification, hyperemia, periappendiceal fat inf

254 ion of CDX2 and ELF5 is not conserved in the mural TE, indicating that although the signals that coor

255 ed in the Rauber's layer, but not in the pig mural TE.

256 n was recorded if no mass was present and if mural thickening (when present) was segmental or diffuse

257 int, level of obstruction, obstructing mass, mural thickening and enhancement, and peritoneal disease

258 Mural thickening demonstrated the greatest interobserver

259 All 16 patients with focal mural thickening had malignant obstruction.

260 Segmental mural thickening occurred in four patients with serosal

261 ss, a disseminated abdominal tumor, or focal mural thickening.

262 resent in four of five patients with diffuse mural thickening.

263 Mural hyperenhancement and increased mural thickness are the most sensitive CT findings of ac

264 s. 0.32 +/- 0.29 mm2; p < 0.05) with smaller mural thrombi (0.03 +/-0.01 mm2 vs. 0.29 +/- 0.30 mm2; p

265 lta 5 mice developed only small, nonoclusive mural thrombi and embolization was limited.

266 Mural thrombi are composed dominantly of platelets and d

267 ently occlusive (<48 hours) and nonocclusive mural thrombi persisted longer in apoE(-/-), PAI-1(+/+)

268 Large mural thrombi were present in 100% of placebo-treated pi

269 FAA markedly reduced platelet deposition, mural thrombi, and injury-induced vasoconstriction after

270 ailure, arrhythmias, and embolic events from mural thrombi.

271 Abciximab treatment alone inhibited mural thrombosis for only 1 day after PTCA, whereas ticl

272 opidine has a prolonged inhibitory effect on mural thrombosis formation relative to either treatment

273 n=26) underwent either carotid crush injury (mural thrombosis model) or embolic stroke (occlusive thr

274 deposition, and the incidence of macroscopic mural thrombosis onto deeply injured artery (tunica medi

275 endothelial cell death and desquamation, and mural thrombosis.

276 egation and the most prolonged inhibition of mural thrombosis.

277 , mitral/tricuspid regurgitation (5), atrial mural thrombus (3), atrial wall thickening (2), and atri

278 histology the control group had evidence of mural thrombus (area 0.8+/-0.4 mm2).

279 Mural thrombus accumulation was present at 4 and 7 days

280 struts per cross section had 50% to 60% less mural thrombus and 2-fold less neointimal area than iden

281 A positive correlation between mural thrombus and dissection area was observed only in

282 II, SEM showed an intimal surface devoid of mural thrombus and platelet aggregates only in Ep + rt-P

283 ipid-rich or fibrous lesions, and luminal or mural thrombus can be readily detected in vivo.

284 A, abciximab/ticlopidine treatment decreased mural thrombus formation to approximately 50% of baselin

285 Mural thrombus formation under arterial shear conditions

286 luded small intracavitary and small or large mural thrombus missed by cine-CMR.

287 leak in 13 (21%), atelectasis in six (10%), mural thrombus within the stent-graft in two (3%), and n

288 rombus or thrombus within dissection planes (mural thrombus), and area measurements were obtained.

289 issed small intracavitary and small or large mural thrombus.

290 latelet aggregation and eliminating residual mural thrombus.

291 new platelet aggregates at sites of residual mural thrombus.

292 nflamed fibrous cap, a dense lipid core, and mural thrombus.

293 cells whose progeny contributes more to the mural trophectoderm and that show compromised developmen

294 late blastocysts that upon dissection of the mural trophectoderm form egg cylinders in only 3 d.

295 evious cleavage cycle tends to contribute to mural trophectoderm.

296 Eight children (24%) harbored the mural-type malformation, and 26 (76%) had the choroidal-

297 Suture disruption or trans-mural vascular tears were not observed.

298 ther agents for gastrointestinal distention, mural visualization, and pancreas-duodenum discriminatio

299 The regions of interest (ROIs) of the murals were manually labeled and grouped into four level

300 Murals with various degrees of flaking were scanned in t