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 e associated with the entire surface of both mural and endothelial cells across all regions of the va

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

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

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

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

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

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 Mural-beta3-integrin loss also enhances tumor growth in

22 linical data correlating high percentages of mural-beta3-integrin-negative tumor BVs with increased t

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

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 primarily on studies of microvascular flow, mural cell control of vessel diameter, and oxygen level-

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

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

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

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

35 Mural cell coverage of the blood vessels was also reduce

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

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

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

39 phatic vessels with reduced and disorganized mural cell coverage.

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

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

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

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

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

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

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

47 PDGFRbeta-dependent signal transduction and mural cell function.

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

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

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

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

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

53 ly in development alongside the emergence of mural cell lineages and persists throughout adulthood ac

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

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

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

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

58 terial, endothelial, venous, angiogenic, and mural cell markers were significantly upregulated in min

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

60 Impaired mural cell migration, differentiation, partial embryonic

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

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

63 bition of TGFbetaR attenuates Myh11+ retinal mural cell myofibroblast differentiation, and diminishes

64 fluid biomarker of BBB-associated capillary mural cell pericyte, soluble platelet-derived growth fac

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

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

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

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

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

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

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

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

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

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

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

76 Mural cell recruitment to the growing endothelial tube i

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

78 solution intravital imaging of the different mural cell subtypes.

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

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

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

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

83 mplish this, we first tested three inducible mural cell-specific mouse lines using a sensitive Ai14 r

84 icyte morphological changes were assessed in mural cell-specific R26-mTmG reporter mice, in which low

85 At a molecular level, mural-cell beta3-integrin loss enhances signaling via FA

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

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

88 In particular, mural-cell-derived CCL2 stimulates tumor cell MEK1-ERK1/

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

90 Mural cells (MCs) are essential for blood vessel stabili

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

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

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

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

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

96 Mural cells (pericytes and vascular smooth muscle cells)

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

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

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

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

101 Mural cells (smooth muscle cells and pericytes) are inte

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

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

104 Mural cells (vascular smooth muscle cells and pericytes)

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

106 ncluding astrocytes, microglia, and vascular mural cells (VMCs).

107 ptional profiles of fibroblasts and vascular mural cells across four murine muscular organs: heart, s

108 Mural cells actively participated during the whole angio

109 n leukocytes, endothelial cells, or arterial mural cells affected the oscillations in a vessel type-s

110 of the CNS, we evaluated distinct classes of mural cells along the vascular tree for both structural

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

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

113 d non-TGFbetaR dependent processes involving mural cells and derived mesenchymal stem cells.

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

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

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

117 n signatures that demarcate fibroblasts from mural cells and provide molecular signatures for cell su

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

119 Mural cells are also recruited by endothelial cells to f

120 Mural cells are emerging as multipotent progenitors of p

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

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

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

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

125 Overall, our data indicate that mural cells can control tumor growth via paracrine signa

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

127 e show that myofibroblast differentiation of mural cells contributes directly to retinal fibrosis.

128 Mouse mural cells demonstrate lower levels of Cd19 expression,

129 te that after chemical ocular injury, Myh11+ mural cells detach from the retinal microvasculature and

130 ansitional segment (TS), which is covered by mural cells distinct from SMCs and pericytes.

131 wed a transient increase in proliferation of mural cells during postnatal maturation.

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

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

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

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

136 Pericytes are a unique class of mural cells essential for angiogenesis, maintenance of t

137 was hypermuscularized, with a hyperplasia of mural cells expressing more contractile proteins, wherea

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

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

140 f the normal function and pathophysiology of mural cells in a variety of disease models.

141 servation has overlooked potential roles for mural cells in directly affecting tumor growth independe

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

143 te the utility of these tools to investigate mural cells in the context of Alzheimer's disease and ce

144 cular coupling is initiated, and the role of mural cells in the control of vasomotility.

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

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

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

148 e functional and structural heterogeneity of mural cells in vivo, and allow detailed cellular studies

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

150 s (NFAT) signaling and APOE in pericyte-like mural cells induces APOE4-associated CAA pathology.

151 lar endothelial cells and the recruitment of mural cells into the cornea.

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

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

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

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

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

157 Pericytes are perivascular mural cells of brain capillaries.

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

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

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

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

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

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

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

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

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

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

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

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

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

171 We identify CD19 expression in brain mural cells using single-cell RNA sequencing data and co

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

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

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

175 cyte, granulosa cells, including cumulus and mural cells), during ovarian follicle development in viv

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

177 oter resulted in sparse TdTomato labeling of mural cells, allowing for an unambiguous characterizatio

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

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

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

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

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

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

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

185 The sphincters are encircled by contractile mural cells, which are capable of bidirectional control

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

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

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

189 Here, we report that mural cells, which surround the endothelium and are crit

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

191 vascular network concentrically wrapped with mural cells.

192 ly expressing a diphtheria toxin receptor in mural cells.

193 in the retinal venous system and associated mural cells.

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

195 ion in pericytes, without affecting arterial mural cells.

196 he outer vessel layer and differentiate into mural cells.

197 formations involving impaired recruitment of mural cells.

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

199 activity of individual and small clusters of mural cells.

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

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

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

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

204 endothelial cells as well as of perivascular mural cells.

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

206 neural activity-evoked calcium transients in mural cells.

207 n homolog deleted on chromosome 10 (PTEN) in mural cells.

208 l origin, including fibroblasts and vascular mural cells.

209 etworks with perfusable lumens surrounded by mural cells.

210 nflammatory and mitogenic status of resident mural cells.

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

212 In 16 subjects mural changes were not found.

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

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

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

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

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

218 he trophectoderm prior to overt polar versus mural differentiation.

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

220 ment of wall thickening (>3 mm), presence of mural edema, perienteric fat stranding, and ulcers were

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

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

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

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

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

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

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

228 In vitro BA production by human mural granulosa cells (MGCs) and cumulus granulosa cells

229 ron microscopy to examine entire cumulus and mural granulosa cells and their projections in mouse ant

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

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

232 Mural granulosa cells were found to possess randomly ori

233 c duodenal injury by differentiating between mural haematoma and a duodenal perforation because the l

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

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

236 Mural hyperenhancement and increased mural thickness are

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 Multivariate analysis demonstrated mural nodularity and atypical cytopathology were predict

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

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

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

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

257 Mass/mural nodule was present in 27% of the cysts, CEA level

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

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

260 ing age, sex, main duct diameter, cyst size, mural nodule, and tumour location were factors considere

261 PCLs) with worrisome features (size >= 3 cm, mural nodule, or Wirsung dilation).

262 eatures, including location, septations, and mural nodules and multiplicity, were noted.

263 Mural nodules can be detected and sampled effectively by

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

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

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

267 Presence of mural nodules, septations, or lesion multiplicity failed

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

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

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

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

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

273 amplifying release and proliferation of the mural pericyte population by ~10-fold.

274 platelet-derived growth factor receptor-beta mural pericytes and subsequent reprogramming into NeuN(+

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

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

277 From these specimens, 6 presented the intra-mural segment, 14 presented the isthmus and 15 presented

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

279 t with loss of luminal epithelial lining and mural stroma necrosis.

280 ing 8/8 luminal, 6/8 intraluminal, and 15/15 mural subtypes) and 74% of AMs (28/38) revealed BRAF V60

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

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

283 ltration, 98% included foreign body, 45% had mural thickening and 20% localized extraluminal air bubb

284 Mural thickening demonstrated the greatest interobserver

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

286 studied including radioopaque foreign body, mural thickness, fatty infiltration or extraluminal air

287 Mural thrombi are composed dominantly of platelets and d

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

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

290 endothelial cell death and desquamation, and mural thrombosis.

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

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

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

294 issed small intracavitary and small or large mural thrombus.

295 Although this might reduce mural-thrombus risk, the relatively more complex vortex

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

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

298 junction, anterior tumors, cT4 tumors, extra-mural venous invasion (EMVI), and threatened or involved

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