ライフサイエンスコーパス: villus

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

2 in the crypt and fully de-methylated in 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 y force that drives cell migration along the villus.

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

8 Therefore, estimates of vagal villus afferent distributions (control minus VAGX) paral

9 Most crypt and villus afferent terminals along the entire proximal-dist

10 Compared with villus afferents, crypt innervation exhibited a muted pr

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

12 p38 MAPK or p53 prevents or rescues ISC and villus aging and nutrient absorption defects.

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

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

15 ated mice exhibited similar distributions of villus and crypt afferents as control mice, suggesting s

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

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

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

19 Both villus and crypt were found to express Vdr and VDR targe

20 Villus and crypts cells were isolated from the rabbit in

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

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

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

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

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

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

27 crypt proliferation and increased crypt and villus apoptosis.

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

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

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

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

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

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

34 f crypt hyperplasia and subsequently blunted villus architecture.

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

36 Stem villus arteries in human IUGR placentas displaying absen

37 ociated with vascular remodeling of the stem villus arteries.

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

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

40 les, with a higher influx of neutrophils per villus at 45I-30R (4.9 [3.1-12.0] vs 3.3 [0.2-4.5]) and

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

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

43 defined by the presence of small intestinal villus atrophy on histopathology specimens during the ye

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

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

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

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

48 ted villus smooth muscle loss and subsequent villus atrophy.

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

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

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

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

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

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

55 1(HI) mesenchymal population lines the crypt-villus axis and is the source of the epidermal growth fa

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

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

58 ression thus accounting for a deranged crypt/villus axis development in CD.

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

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

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

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

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

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

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

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

67 tion of epithelial gene expression along the villus axis, but the mechanisms shaping this spatial var

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

69 helial spatial expression programs along the villus axis.

70 fferentiation of enterocytes along the crypt-villus axis.

71 itors, compared with other cells along crypt-villus axis.

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

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

74 lations of mesenchymal cells along the crypt-villus axis.

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

76 and augments cellular progression along the villus axis.

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

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

79 hi) telocytes are especially abundant at the villus base and provide a BMP reservoir, and we identifi

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

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

82 Villus blunting and heavy inflammatory infiltrates were

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

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

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

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

87 Environmental enteropathy (EE) refers to villus blunting, reduced absorption, and microbial trans

88 consisting of attenuation of the mucosa with villus blunting.

89 and reduced histopathological damage such as villus blunting.

90 nflammation that is associated with moderate villus blunting.

91 nflammatory pathways in C57BL/6 mice without villus blunting.

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

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

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

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

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

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

98 Inhibition of intestinal villus cell Na/K-ATPase mediates altered glucose and NaC

99 In vivo, during obesity inhibition of villus-cell BLM, Na/K-ATPase led to compensatory stimula

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

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

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

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

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

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

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

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

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

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

110 Crypt and villus cells were isolated, incubated with fluorescently

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

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

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

114 These genes, derepressed in PRC2-null villus cells, remain silent in intestinal stem cells (IS

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

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

117 ontain both intestinal stem cells and mature villus cells.

118 ently than transit amplifying progenitors or villus cells.

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

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

121 were dramatically increased in pRb-deficient villus cells.

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

123 change in the brush border membrane (BBM) of villus cells.

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

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

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

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

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

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

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

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

132 e have established early-gestation chorionic villus-derived placenta mesenchymal stromal cells (PMSCs

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

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

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

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

137 receptor previously shown to participate in villus development.

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

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

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

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

142 The villus dysmorphogenesis is independent of alterations in

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

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

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

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

147 sorganized and temporarily stratified during villus emergence.

148 ubepithelial mesenchymal clusters that drive villus emergence.

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

150 Villus enterocyte nutrient absorption occurs via precise

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

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

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

154 Villus enterocytes were OTR-immunoreactive through postn

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

156 fically impaired viability and maturation of villus enterocytes.

157 nently localizes to the luminal interface of villus enterocytes.

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

159 al accumulation of intracellular vesicles in villus enterocytes.

160 illi length on the surface of crypt, but not villus, enterocytes.

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

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

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

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

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

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

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

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

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

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

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

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

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

174 reas EGF is expressed far from crypts in the villus epithelium.

175 ty is evident in differentiated, postmitotic villus epithelium.

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

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

178 Exposure of villus explants to hypoxia-reoxygenation significantly r

179 In villus explants, IgG-virion transcytosis and macrophage

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

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

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

183 Synovial villus formation or inflammatory cell infiltration was s

184 mice, we demonstrate their critical roles in 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 k we observed an effect of micronutrients on villus height (VH).

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

194 Villus height and crypt perimeter were significantly dec

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 We measured villus height, crypt perimeter, and relative densities o

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 developed a fatal GI pathology with dramatic villus hypoplasia.

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

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

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

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

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

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

214 erate mesentery-to-antimesentery decrease in villus innervation.

215 epithelial cells from the non-proliferative villus into the proliferative intervillus region, which

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

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

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

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

220 s and their progeny differentiate near crypt-villus junctions.

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

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

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

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

225 decreased crypt proliferation and shortened villus length.

226 ration and migration, resulting in increased villus length.

227 -Jun resulted in decreased proliferation and villus length.

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

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

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

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

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

233 Areas of villus loss became complicated by spontaneous inflammati

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

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

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

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

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

239 During villus morphogenesis, intervillus cells proliferate acti

240 and Sox9 expression that accompanies normal villus morphogenesis.

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

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

243 The inter-villus mucus was less heterogeneous than the mucus cover

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

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

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

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

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

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

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

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

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

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

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

255 with available clinical data from chorionic villus sampling (CVS) or amniocentesis procedures.

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

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

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

259 Villus shortening was preceded by increased caspase 3 an

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

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

262 the small intestinal mucosa with significant villus shortening.

263 activity of intestinal stem cells as well as villus size and density.

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

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

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

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

268 ative and undifferentiated stage to a mature villus stage.

269 intestinal crypt progenitor/stem (ICPS) and villus stromal cells through induction of Bcl-2 family-m

270 Here, we show that aging-caused intestinal villus structural and functional decline is regulated by

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

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

273 ression of claudin-2 increased from crypt to villus tip (P < .001) and was up-regulated in CLE(+) pat

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

275 VTTs are elongated cells that line the villus tip epithelium and signal through Bmp morphogens

276 These include villus tip telocytes (VTTs) that express Lgr5, a gene pr

277 he small intestinal stroma and exposes Lgr5+ villus tip telocytes as regulators of the epithelial spa

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

279 of infected enterocytes until they reach the villus tip.

280 zonation of enterocyte genes induced at the villus tip.

281 ts vs controls (P = .022) and were lowest in villus tips (P < .001).

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

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

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

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

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

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

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

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

290 ubsequent apoptosis of effete cells from the villus tips.

291 fferentiate and are ultimately shed from the villus tips.

292 fragment that is spatially restricted to the villus tips.

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

294 g, we find that during fetal development the villus undergoes gross remodelling and fission.

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

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

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