ライフサイエンスコーパス: villus

1 in the crypt and fully de-methylated in the villus.

2 y force that drives cell migration along the villus.

3 a function of the number of capillaries per villus.

4 elated to the number of capillaries within a villus.

5 38N/+) mice compared with WT, but not in the villus.

6 ion in the crypts and differentiation on the villus.

7 restrict the stem cells to the base of each villus.

8 gnals, in particular Shh, at the tip of each villus.

9 d numbers of goblet cells, and detachment of villus absorptive cells from the villus core as intact s

10 One population of fibers, the villus afferents, supplies plates of varicose endings to

11 development, abrogated these changes in the villus and colon cells.

12 lung alveolarization, atrophy of intestinal villus and colon-resident lymphoid follicle, and degener

13 In contrast, villus and crypt apoptosis were increased in septic fabp

14 BBM vesicles (BBMV) were prepared from villus and crypt cells and uptake studies were performed

15 Expression profiles in villus and crypt epithelium were determined by DNA micro

16 ness in the extent of recombination and that villus and crypt populations could be targeted different

17 Villus and crypts cells were isolated from the rabbit in

18 els located at the center of each intestinal villus and provide essential transport routes for lipids

19 ber of infected epithelial cells present per villus and significantly exacerbated oocyst excretion.

20 ly inflamed intestine, may regulate B0AT1 in villus and SN2/SNAT5 in crypt cell is unknown.

21 s defined as the ratio of oxygen flux into a villus and the sum of the capillary areas contained with

22 hat Rspo1 improved mucosal integrity in both villus and/or crypt compartments in the small intestine

23 apoptosis but had a paradoxical increase in villus apoptosis compared with septic fabpi-TAg mice, as

24 opic enterocyte proliferation with increased villus apoptosis in unmanipulated animals.

25 crypt proliferation and increased crypt and villus apoptosis.

26 nt of the isolated fibers indicated that the villus arbors and the crypt endings are independent, iss

27 ars to represent a new mechanism controlling villus architectural organization.

28 dynamics that determine the epithelial crypt-villus architecture across a range of conditions from he

29 estinal stem cells contributing to the crypt-villus architecture and a laminated human mesenchyme, bo

30 At E18.5, intestinal villus architecture and epithelial cell populations were

31 rophic crypt loss and deterioration of crypt-villus architecture.

32 f crypt hyperplasia and subsequently blunted villus architecture.

33 lete picture of oxygen fluxes, capillary and villus areas is obtainable and presents an opportunity f

34 Stem villus arteries in human IUGR placentas displaying absen

35 ociated with vascular remodeling of the stem villus arteries.

36 be recapitulated in vitro by subjecting stem villus artery explants to hypoxia-reoxygenation, or inhi

37 rom stem cells in the crypts, migrate up the villus as they differentiate and are ultimately shed fro

38 stine (i.e., duodenum), including widespread villus atrophy and epithelial damage.

39 Upon shRNA withdrawal, villus atrophy and weight loss were fully reversible.

40 llus length compared with sham mice, whereas villus atrophy was further exacerbated in septic Vil-Cre

41 pecific RIPK1 knockout caused IEC apoptosis, villus atrophy, loss of goblet and Paneth cells and prem

42 gen of intestinal epithelium that results in villus atrophy, mucosal lipid peroxidation, diarrhea, an

43 act on the severity of epithelial infection, villus atrophy, or diarrhea.

44 ted villus smooth muscle loss and subsequent villus atrophy.

45 ation along the anterior-posterior and crypt-villus axes, and mechanisms of epithelial differentiatio

46 during their migration along the mouse crypt-villus axis (CVA).

47 tains a Cu gradient along the duodenal crypt-villus axis and buffers Cu levels in the cytosol of ente

48 d the distribution of miRNAs along the crypt-villus axis and changed the miRNA profiles of both villi

49 interactions position cells along the crypt-villus axis and compartmentalize incipient colorectal tu

50 wing of enterocyte migration along the crypt-villus axis and focal mucosal injury.

51 egulated miRNAs and proteins along the crypt-villus axis are highly related to this process.

52 ession and function of PepT1 along the crypt-villus axis demonstrated that this protein is crucial to

53 shows an expression gradient along the crypt-villus axis in the normal human intestine.

54 The crypt-villus axis is composed of a dynamic cell population in

55 tion of the epithelial cells along the crypt-villus axis segregates them into regions of specialized

56 ells distribute in a pattern along the crypt-villus axis similar to long-term label-retaining cells (

57 exchange is concentrated in the lower crypt-villus axis where it is subject to Cftr regulation.

58 d differentiation take place along the crypt-villus axis, and are controlled by the Wnt and hedgehog

59 s relative to their position along the crypt-villus axis, and the levels of cyclins, cyclin-dependent

60 on for each of the compounds along the crypt-villus axis, as well as confirming a proximal-distal abs

61 he migration of enterocytes across the crypt-villus axis, by regulating CD98 expression.

62 l epithelial cell maturation along the crypt-villus axis, enterocytes were sequentially isolated from

63 ure enterocytes while moving along the crypt-villus axis.

64 ate epithelial cell dynamics along the crypt-villus axis.

65 al epithelial cell migration along the crypt-villus axis.

66 ests a role for GC-C in organizing the crypt-villus axis.

67 and augments cellular progression along the villus axis.

68 yuridine-labeled enterocytes along the crypt-villus axis.

69 fferentiation of enterocytes along the crypt-villus axis.

70 ds represent distinct points along the crypt-villus axis; they can be used to characterize electrolyt

71 ds to lethal intestinal pathology, including villus blunting and death of intestinal crypts, and loss

72 g necrosis of epithelium and lamina propria, villus blunting and fusion, and transmural edema and hem

73 Villus blunting and heavy inflammatory infiltrates were

74 nd reduced STEC-induced histological damage (villus blunting).

75 hyperplasia, muscularis propria hypertrophy, villus blunting, and expression of inflammatory and remo

76 ation of intestinal epithelial architecture (villus blunting, goblet cell hyperplasia, and increased

77 in the duodenal and colonic mucosa including villus blunting, increased lamina propria and intraepith

78 consisting of attenuation of the mucosa with villus blunting.

79 and reduced histopathological damage such as villus blunting.

80 s is independent of alterations in the crypt-villus boundary and inappropriate beta-catenin activatio

81 resulting in expression of both genes in the villus but Bcl-2 alone in the crypt.

82 the initial aspects of the formation of each villus by controlling mesenchymal cluster aggregation an

83 sence or presence of Bb12 also increased the villus cell height in the proximal colon along with a tr

84 is required for maintaining the postmitotic villus cell in quiescence, governing the expression of c

85 Nor is it known precisely how villus cell migration is affected when proliferation is

86 M) Na-glutamine co-transport is inhibited in villus cells (mediated by B0AT1), while it is stimulated

87 villin is highest in the apoptosis-resistant villus cells and lowest in the apoptosis-sensitive crypt

88 ependent glutamine co-transporters, B0AT1 in villus cells and SN2 in crypts cells that are uniquely a

89 pRb-deficient villus cells appeared capable of progressing to mitosis

90 icating an active promoter, was prevalent in villus cells but barely detectable in crypt cells.

91 etotifen reversed the inhibition of B0AT1 in villus cells by restoring co-transporter numbers in the

92 The dietary-induced changes in villus cells encompassed ectopic expression of Paneth ce

93 absorption of nutrients and electrolytes by villus cells is decreased with a concomitant increase in

94 sms and, in mammals, is absorbed through the villus cells of the duodenum.

95 ed gene expression profiles predominantly in villus cells of the histologically normal mucosa, in con

96 D44 and cyclinD1 are expressed in late fetal villus cells that show high Wnt activity.

97 ntegrin staining in the lateral membranes of villus cells, and this pattern was accentuated in Rab25-

98 gnificant increases in intracellular cAMP in villus cells, but not in crypt cells.

99 In villus cells, Na-glutamine co-transport inhibition obser

100 In primary intestinal villus cells, we identified hundreds of tissue-restricte

101 et cell differentiation were up-regulated in villus cells, whereas Paneth cell markers were maximally

102 restored immune-reactive levels of B0AT1 in villus cells, while SN2/SNAT5 levels from crypts cell re

103 ontain both intestinal stem cells and mature villus cells.

104 ently than transit amplifying progenitors or villus cells.

105 rypt bottom), and increased Wnt signaling in villus cells.

106 candidate for CD98, than well-differentiated villus cells.

107 were dramatically increased in pRb-deficient villus cells.

108 , p57, and p16 was highest in differentiated villus cells.

109 ignaling center called the "villus cluster." Villus cluster signals, notably Bmp4, feed back on the o

110 chyme to form a signaling center called the "villus cluster." Villus cluster signals, notably Bmp4, f

111 ncreasing Hh signaling increases the size of villus clusters and results in exceptionally wide villi.

112 were all significantly higher in intestinal villus compared with crypt epithelial cells.

113 tachment of villus absorptive cells from the villus core as intact sheets.

114 onsive cells and Hh levels actively modulate villus core smooth muscle.

115 phoblasts, then reaches blood vessels in the villus core.

116 ial myofibroblasts, loss of smooth muscle in villus cores and muscularis mucosa as well as crypt hype

117 testinal epithelial cell migration along the villus/crypt axis, altered intestinal morphology, and dy

118 rn of CMV replication proteins in underlying villus cytotrophoblasts, whereas syncytiotrophoblasts we

119 lacking caspase 8 in IECs but instead caused villus destruction with a loss of small intestinal surfa

120 e intestinal epithelium during the period of villus development and epithelial cytodifferentiation, t

121 Hh signaling prevents cluster formation and villus development, but does not prevent emergence of vi

122 During murine villus development, epithelial Hedgehog (Hh) signals pro

123 receptor previously shown to participate in villus development.

124 t Yin Yang 1 (Yy1) is crucial for intestinal villus development.

125 he chronic inflammatory index ( P < .01) and villus distortion index ( P < .01) in the ileum of SAMP1

126 (ISCs) become localized to the base of each villus during embryonic development.

127 type homeobox gene, Cdx2, leading to obvious villus dysmorphogenesis and severely disrupted epithelia

128 ulated beta-catenin activation causes severe villus dysmorphogenesis in transgenic mice.

129 The villus dysmorphogenesis is independent of alterations in

130 ration, increased epithelial transit, severe villus dysmorphogenesis, and crypt dysmorphogenesis.

131 sphorylation gene expression at the onset of villus elongation, suggesting that aerobic respiration m

132 ters, promoting approximately four rounds of villus emergence by E18.5.

133 We find that, before villus emergence, tight clusters of Hh-responsive mesenc

134 sorganized and temporarily stratified during villus emergence.

135 ubepithelial mesenchymal clusters that drive villus emergence.

136 deficiency results in loss of resistance of villus endothelial and lymphocyte populations to radiati

137 However, we recently showed that villus endothelium expressed a separate FcR for IgG, the

138 ammaRIIb-mediated transfer of IgG across the villus endothelium, independent of caveolae.

139 entifiable and likely novel organelle of the villus endothelium, unassociated with caveolae.

140 The second layer, the villus endothelium, was until recently thought to allow

141 , with particular exaggeration of defects in villus enterocyte differentiation.

142 Villus enterocyte nutrient absorption occurs via precise

143 rated mice with conditional Mttp deletion in villus enterocytes (Mttp-IKO), using a tamoxifen-inducib

144 Villus enterocytes from chow-fed Mttp-IKO mice contained

145 Bcl-w messenger RNA expression in crypt and villus enterocytes in control conditions and under epide

146 as well as ectopic cell cycle reentry within villus enterocytes in the small intestine.

147 However, the cycling villus enterocytes were not completely differentiated as

148 Villus enterocytes were OTR-immunoreactive through postn

149 ctivate transcription of the Slc6a19 gene in villus enterocytes, whereas high levels of SOX9 repress

150 nently localizes to the luminal interface of villus enterocytes.

151 ice that express a J domain mutant (D44N) in villus enterocytes.

152 could not detect T antigen/p53 complexes in villus enterocytes.

153 f TIS7 into small intestinal upper crypt and villus enterocytes.

154 al accumulation of intracellular vesicles in villus enterocytes.

155 fically impaired viability and maturation of villus enterocytes.

156 l gene expression patterns between crypt and villus epithelial cell lineages in human ileal tissue pr

157 We have identified a pathway by which villus epithelial cells are maintained during C parvum i

158 intestinal epithelial Caco-2 cells and crypt/villus epithelial cells isolated from wild-type and tran

159 In adult mice, PTK6 expression is high in villus epithelial cells of the small intestine.

160 tion and localized to the apical membrane of villus epithelial cells.

161 r localization of the Akt substrate FoxO1 in villus epithelial cells.

162 aser capture microdissection from either the villus epithelial or crypt cell regions of healthy human

163 Endogenous Rspo1 protein was localized to villus epithelium and crypt Paneth cells in mouse small

164 the porcine GLP-2R mRNA was expressed in the villus epithelium and myenteric plexus.

165 normally secreted from the small intestinal villus epithelium and suppressed by the microbiota, show

166 intestinal stem cells and mature intestinal villus epithelium correlated with expression levels of a

167 ent in the lamina propria under the columnar villus epithelium of the small bowel extend processes ac

168 Hic-5 and PPARgamma colocalize to the villus epithelium of the small intestine, and their expr

169 subepithelial DCs into the FAE, but not into villus epithelium of wild-type and TLR4-deficient mice.

170 show that TLR2 is expressed in both FAE and villus epithelium, but TLR2 activation by peptidoglycan

171 ty is evident in differentiated, postmitotic villus epithelium.

172 igands in a manner that is distinct from the villus epithelium.

173 upregulation of IFN-responsive genes in the villus epithelium.

174 lary number, caliber and position within the villus-even in placentas deemed clinically "normal".

175 correlate with crypt enlargement and marked villus expansion and/or damage.

176 Infection of villus explants and differentiating and/or invading cyto

177 Exposure of villus explants to hypoxia-reoxygenation significantly r

178 In villus explants, IgG-virion transcytosis and macrophage

179 with a concomitant increase in crypt and/or villus fluid secretion.

180 r, and transcellular permeabilities, and the villus-fold surface area expansion factor (k(VF)).

181 Here, we analyze the cell biology of villus formation and examine the role of paracrine epith

182 Villus formation in the small intestine was affected and

183 Synovial villus formation or inflammatory cell infiltration was s

184 signal compromises epithelial remodeling and villus formation.

185 The intestines display villus fusion, apical membrane blebs, and disrupted micr

186 before or after villus morphogenesis yields villus fusion, revealing a previously unrecognized step

187 Mitochondrial inhibitors blocked villus growth in a fashion similar to Yy1 loss, thus fur

188 respiration might function as a regulator of villus growth.

189 intestinal epithelial cell proliferation and villus growth.

190 intestinal injury, as evidenced by decreased villus height and a compensatory shift in proliferating

191 -fed animals, increases in ileum and jejunum villus height and crypt depth were observed in compariso

192 thelial renewal based on BrdU incorporation, villus height and crypt depth, and cell number.

193 reased crypt cell proliferation and enhanced villus height and crypt depth, resulting in augmented in

194 r resection, adaptation results in increased villus height and crypt depth.

195 This study shows that AA-ORS increased villus height and improved electrolyte and nutrient abso

196 leal mucosal DNA and protein levels, greater villus height in jejunum and ileum and crypt depth in il

197 The ratio of villus height to crypt depth and densities of intraepith

198 mucosal injury after gluten challenge (mean villus height to crypt depth ratio changed from 2.8 befo

199 Significant differences in villus height, crypt depth, dry mass, and concentrations

200 eight, p < 0.04 crypt depth; ileum p < 0.001 villus height, p < 0.002 crypt depth).

201 arison to sow-fed animals (jejunum, p < 0.01 villus height, p < 0.04 crypt depth; ileum p < 0.001 vil

202 No changes in villus height/crypt depth were observed.

203 overall En/Erm phenotype of disturbed crypt-villus homeostasis is consistent with recently identifie

204 results in marked disruption of normal crypt-villus homeostasis, including a cell-autonomous disturba

205 wth, associated with crypt fission and crypt/villus hyperplasia, respectively, which subsequently pre

206 ransgene increased ISC numbers and triggered villus hypertrophy.

207 on of Robo1 decreased ISC numbers and caused villus hypotrophy, whereas a Slit2 transgene increased I

208 eta protected crypt IECs but did not protect villus IECs from dsRNA-induced or TNF-induced apoptosis.

209 ps and then progressively affects the entire villus, including necrosis of epithelium and lamina prop

210 that are necessary and sufficient to induce villus injury and compromise intestinal barrier function

211 biotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria.

212 MA KO mice show no protection from crypt and villus injury or recovery after 15 or 12 Gy TBI, but hav

213 iency and the number of capillaries within a villus is established.

214 Using a newly developed crypt/villus isolation method, we uncovered that expression of

215 that (a) down-regulation of Id1 at the crypt/villus junction coincides with PKCalpha activation, and

216 lands or crypts, immediately below the crypt-villus junction.

217 stricted to crypts and concentrated at crypt-villus junctions.

218 ge of absorbed molecules in small intestinal villus lacteals and the involvement of lacteal contracti

219 utrophil influx and extravasation within the villus lamina propria microenvironment.

220 ugh exposure to UFP further led to shortened villus length accompanied by prominent macrophage and ne

221 Septic wild-type mice had decreased villus length compared with sham mice, whereas villus at

222 ration and migration, resulting in increased villus length.

223 -Jun resulted in decreased proliferation and villus length.

224 decreased crypt proliferation and shortened villus length.

225 ncreased bromodeoxyuridine incorporation and villus lengthening, changes that did not occur in apoB10

226 elding decreased crypt markers and increased villus-like characteristics.

227 ved in patients with AD, including prominent villus-like projections (VP); however, these ultrastruct

228 columnar epithelium that was patterned into villus-like structures and crypt-like proliferative zone

229 ntiated or crypt-like, and differentiated or villus-like, human enteroids represent distinct points a

230 Areas of villus loss became complicated by spontaneous inflammati

231 apamycin complex 2 also contributes to ileal villus maintenance and goblet cell size.

232 Finally, crypt-to-villus migration rates are unchanged in CASK-deficient i

233 Shh promoter resulting in the inhibition of villus morphogenesis and epithelial differentiation.

234 nic foregut results in reversible defects in villus morphogenesis and loss of the proliferative proge

235 testinal epithelium, resulting in incomplete villus morphogenesis and neonatal death.

236 ly, deletion of Ezrin either before or after villus morphogenesis yields villus fusion, revealing a p

237 During villus morphogenesis, intervillus cells proliferate acti

238 and Sox9 expression that accompanies normal villus morphogenesis.

239 de novo lumen formation and expansion during villus morphogenesis.

240 Although villus morphology appeared normal at E16.5, the first ti

241 titive deformation induced by peristalsis or villus motility may support the gut mucosa by a pathway

242 Ex vivo analysis of transgenic crypt-villus organoid cultures revealed an increased prolifera

243 vidual differences in expression patterns in villus parenchyma and systematic differences between the

244 on, chorion, umbilical cord, and sections of villus parenchyma from 19 human placentas from successfu

245 The umbilical cord, chorion, amnion, and villus parenchyma samples were readily distinguished by

246 was expressed in both the maternal and fetal villus parenchyma sections of placenta included genes th

247 Thus, unlike in chick, the murine villus patterning system is independent of muscle-induce

248 ngly, modest attenuation of Hh also perturbs villus patterning.

249 fabpi-TAg mice had an unexpected increase in villus proliferation compared with unmanipulated litterm

250 o the abundant presence of receptors in this villus region, and (iii) claudin-4 being an important in

251 of claudin-4, a known CPE receptor, in this villus region.

252 em cells generated numerous long-lived crypt-villus "ribbons," indicative of dedifferentiation of ent

253 bmitted data for amniotic fluid or chorionic villus samples referred from April, 1999, to March, 2004

254 Of 34,995 amniotic fluid and 3049 chorionic villus samples that had karyotyping and a rapid test on

255 fluid samples and 152 (45%) of 327 chorionic villus samples were associated with a substantial risk o

256 119,528 amniotic fluid and 23,077 chorionic villus samples, rapid aneuploidy testing replacement of

257 agnosed with del(4)(q33) following chorionic villus sampling (CVS) at 14 weeks, and the pregnancy was

258 We did a cost-utility analysis of chorionic villus sampling and amniocentesis versus no invasive tes

259 e cells from the amniotic fluid or chorionic villus sampling that are used for prenatal diagnosis, we

260 yos, (ii) induced abortions, (iii) chorionic villus sampling, (iv) amniocentesis, and (v) fetal death

261 e early caspase 3 activation with subsequent villus shortening in mice lacking caspase 8 in IECs but

262 Villus shortening was preceded by increased caspase 3 an

263 protected from dsRNA-induced IEC apoptosis, villus shortening, and diarrhea.

264 Exposure to UFP promotes lipid metabolism, villus shortening, and inflammatory responses in mouse s

265 the small intestinal mucosa with significant villus shortening.

266 ; and after birth, the muscularis mucosa and villus smooth muscle consist primarily of Hedgehog-respo

267 ix- to 10-month-old VFHhip animals exhibited villus smooth muscle loss and subsequent villus atrophy.

268 epithelium leads to progressive expansion of villus smooth muscle, but does not result in reduced epi

269 ng events involving the serosa, pylorus, and villus smooth muscle.

270 ative and undifferentiated stage to a mature villus stage.

271 ar beta-catenin translocation, loss of crypt-villus structure, and impaired barrier function.

272 ding cells were diffusely distributed on the villus surface.

273 n the incoming oxygen flow and the absorbing villus surface.

274 The numbers of IELs in the villus tip and sides were counted and the quotient tip/s

275 erocytes were sequentially isolated from the villus tip to the crypts of mouse small intestine.

276 on of epithelial cells from the crypt to the villus tip.

277 of infected enterocytes until they reach the villus tip.

278 lial lining, but extensive damage in jejunal villus tips after 60 minutes ischemia.

279 ng with severe mucosal damage that starts at villus tips and then progressively affects the entire vi

280 enterotoxicity, (ii) the CPE sensitivity of villus tips being at least partially attributable to the

281 results in global changes in polarity at the villus tips that could account for deficits in apical ab

282 ntirely of enterocytes and are all lost from villus tips within days.

283 leavage, enterocyte shedding was confined to villus tips, coincident with apoptosis, and observed mor

284 ealed strong CPE or rCPE(168-319) binding to villus tips, which correlated with the abundant presence

285 ath at the colon surface or small intestinal villus tips.

286 ubsequent apoptosis of effete cells from the villus tips.

287 sed, and ectopic precrypt structures form on villus tips.

288 fferentiate and are ultimately shed from the villus tips.

289 fragment that is spatially restricted to the villus tips.

290 s as well as the sloughing of cells from the villus tips.

291 Ets factors in the homeostasis of the crypt-villus unit, the functional unit of the small intestine.

292 th and intermediate cells along the crypt-to-villus unit.

293 s with resultant labeling of an entire crypt-villus unit.

294 , is necessary for preservation of the crypt-villus unit.

295 ocytes at the time of formation of the crypt-villus unit.

296 uced proliferation in small intestinal crypt-villus units from compound Apc(min/+) apobec-1(-/-) mice

297 pithelium is a repetitive sheet of crypt and villus units with stem cells at the bottom of the crypts

298 Each villus was approximately 100 nm in diameter and 600 to 1

299 fferentially expressed between the crypt and villus were identified.

300 significantly lower ileal mitotic index and villus width, and significantly increased intestinal IFN

301 ial cells (IECs) located in the mid to upper villus with ensuing luminal fluid accumulation and diarr