ライフサイエンスコーパス: ENS

1 ENS cells originate from vagal and sacral neural crest c

2 ENS cells were cultured under proliferation conditions l

3 ENS ganglia exist as a collection of neurons and glia th

4 ENS infection led to robust viral gene transcription, pa

5 ENS neurons across multiple mammalian species express Ca

6 ENS precursors derived in vitro are capable of targeted

7 ENS structural and functional anomalies were completely

8 ENS-containing HIOs grown in vivo formed neuroglial stru

9 unicate with the ENS, integrating data about ENS function into a broader view of human health and dis

10 r colon that provides more information about ENS structure than tissue sectioning.

11 t colonic microbiota help maintain the adult ENS via a specific signaling pathway.

12 bacteria or their products affect the adult ENS via toll-like receptors (TLRs) in mice.

13 ppear to innervate and activate in the adult ENS.

14 , small molecules, and nutrients that affect ENS morphogenesis and mature function.

15 We found that zebrafish lacking an ENS due to a mutation in the Hirschsprung disease gene,

16 The absence of an ENS from variable lengths of the colon results in Hirsch

17 eems to be associated with a better anchored ENS and better mapping abilities between ENS and ANS.

18 ice had abnormalities in ENS development and ENS-mediated GI functions, including reduced motility an

19 After comparing ECS and ENS, we describe a few representative examples where nat

20 the molecular processes underpinning gut and ENS development, we generated RNA-sequencing profiles fr

21 migration and failure to form an appropriate ENS.

22 red ENS and better mapping abilities between ENS and ANS.

23 4 h it was no significant difference between ENS and CLN.

24 The implanted device captures ENS responses to neurotransmitters, drugs and optogeneti

25 o have a better understanding of the colonic ENS.

26 lates intestinal inflammation by controlling ENS structure and neurochemical coding, along with intes

27 roliferation and differentiation of cultured ENS progenitor cells from neonatal mice and humans.

28 defects are unlikely to be due to defective ENS precursor migration since R1(KO)R2(Het)R3(KO) mice h

29 We propose that Nav-dependent ENS disorders of excitability may play important roles i

30 tment and migration of human PS-cell-derived ENS precursors rescue disease-related mortality in HSCR

31 ice overexpressing mutant human aSyn develop ENS pathology by 4 months.

32 erived Shh acts indirectly on the developing ENS by regulating the composition of the intestinal micr

33 Indeed, Smn deficiency led to disrupted ENS signaling to the smooth muscle of the colon but did

34 atory transcription factors described during ENS development.

35 not necessary to guide migrating ENCC during ENS development.

36 h NCC interact with their environment during ENS development.

37 n; and if it is ectopically expressed during ENS development, such SRY repression could result in RET

38 ght the crucial roles played by Foxd3 during ENS development including progenitor proliferation, neur

39 a late temporal requirement for Foxd3 during ENS development.

40 d form distinct connectivity patterns during ENS development.

41 process of specific neuronal subtypes during ENS development.

42 ChR subunits to synaptic transmission during ENS development, even after birth.

43 neurons have been detected in the embryonic ENS; however, the development of these neurons has been

44 ll diversity is created within the embryonic ENS; information required for development of cell-based

45 of ENS within the past decade and emphasize ENS for functions.

46 te the inter-relationship of migrating ENCC, ENS formation and gut vascular development we combined f

47 d RNA expression profiles of the entire ENS, ENS progenitor cells, and non-ENS gut cells of mice, col

48 mpared RNA expression profiles of the entire ENS, ENS progenitor cells, and non-ENS gut cells of mice

49 Here we review studies evaluating ENS defects in HSCR and non-HSCR mouse models, concludin

50 Focal ENS ablation leads to increased smooth muscle and mucosa

51 ed values of ENS density vary up to 150-fold-ENS density varies greatly, across millimeters, so analy

52 Weanlings grouped distinctly for ENS and IUGR by partial least-squares discriminate analy

53 the relative importance of these enzymes for ENS development, we analyzed whole mount preparations of

54 CLN, NUP98, and TBATA) are indispensable for ENS development in zebrafish, and these results were con

55 al lineages provides a powerful platform for ENS-related disease modeling and drug discovery.

56 In proliferating enterospheres derived from ENS progenitor cells, we verified the expression of Wnt

57 -derived intestinal tissue with a functional ENS and how this system can be used to study motility di

58 an intestinal tissue containing a functional ENS.

59 ifferentiation in order to form a functional ENS.

60 Although development of a fully functional ENS is required for gastrointestinal motility, little is

61 echanisms and cellular processes that govern ENS development, identify areas in which more investigat

62 e mice depleted of intestinal microbiota had ENS defects and GDNF deficiency, similar to Tlr2(-/-) mi

63 e ENs, we transcriptionally profiled healthy ENS from adult humans and mice.

64 Human ENS development remains poorly understood owing to the l

65 l analyses of the developing mouse and human ENS, we mapped expression patterns of transcription and

66 electrical activity in the developing human ENS.

67 Of the factors also analyzed in human ENS, most were conserved.

68 S-cell-based platform for the study of human ENS development, and presents cell- and drug-based strat

69 could provide targets for treatment of human ENS disorders.

70 ol provides access to a broad range of human ENS lineages within a 30-d period.

71 The human ENS expresses risk genes for neuropathic, inflammatory,

72 gs identified in a zebrafish screen impaired ENS development.

73 mycophenolate treatment selectively impaired ENS precursor proliferation, delayed precursor migration

74 TPH2-R439H mice had abnormalities in ENS development and ENS-mediated GI functions, including

75 Tlr2(-/-) mice had alterations in ENS architecture and neurochemical profile, intestinal d

76 r de novo guanine nucleotide biosynthesis in ENS development and suggest that some cases of HSCR may

77 m enteric neurons that results in defects in ENS development and GI motility.

78 Defects in ENS development are responsible for many human disorders

79 irst evidence that developmental deficits in ENS wiring may contribute to the pathogenesis of idiopat

80 Perturbations in ENS development or function are common, yet there is no

81 ng IUGR lineage F2 offspring was reversed in ENS (P < 0.04).

82 e diagnosis of diseases linked to incomplete ENS formation, such as Hirschsprung's disease.

83 nd that exogenous NO and Rb1 shRNA increased ENS precursor DNA replication and nuclear size.

84 We recapitulated normal intestinal ENS development by combining human-PSC-derived neural cr

85 udies in this area promise new insights into ENS physiology and pathophysiology.

86 or focal intestinal perforation and isolated ENS cells.

87 We isolated ENS progenitors from tunica muscularis of the small inte

88 Conversely, in miRet(51) mice, which lack ENS in the hindgut, the vascular network in this region

89 T transgenic (Tg) mice closely model PD-like ENS aSyn pathology, making them appropriate for testing

90 Conversely, IUGR lineage ENS-fed rats did not manifest MetS, with significantly l

91 first medicine identified that causes major ENS malformations and Hirschsprung-like pathology in a m

92 ase, raising the possibility that microbiota-ENS interactions could offer a viable strategy for influ

93 ss collagen VI in the intestine by migrating ENS precursors as they colonize fetal bowel.

94 sema3 knockdowns show reduction of migratory ENS precursors with complete ablation under conjoint ret

95 lent bonds to generate individual molecules, ENS is a unifying theme for understanding the functions,

96 induced to occur in vivo in the adult mouse ENS.

97 In studies of human and mouse ENS progenitors, we found activation of the Wnt signalin

98 considered when relating findings from mouse ENS research to human gastrointestinal studies.

99 proteins are also expressed within the mouse ENS and their expression is also lost in the ENS of Ret-

100 he amorphous neuroglia networks of the mouse ENS are composed of overlapping clonal units founded by

101 cally defined cellular circuits of the mouse ENS, together with the functional contribution of GABAAR

102 l expression during development of the mouse ENS.

103 Finally, EDNRB-null mutant ENS precursors enable modelling of HSCR-related migratio

104 Here, we demonstrate that the non-neuronal ENS cell compartment of teleosts shares molecular and mo

105 he entire ENS, ENS progenitor cells, and non-ENS gut cells of mice, collected at embryonic days 11.5

106 loping gut tissues, are important for normal ENS development and its disorders.

107 Retinoids are essential for normal ENS development, but the role of retinoic acid (RA) meta

108 Analyses of ENS-lineage and differentiation in mutant embryos sugges

109 The spatial configuration of ENS clones depends on proliferation-driven local interac

110 determined in a medium of primary culture of ENS and neuro-glial coculture model treated by lipopolys

111 ignificantly increased on primary culture of ENS treated with LPS.

112 After that, we introduce the exploration of ENS of man-made molecules in the context of cells by dis

113 CR is caused by the developmental failure of ENS progenitors to migrate into the gastrointestinal tra

114 the canonical Wnt pathway promoted growth of ENS cell spheres during cell expansion and increased the

115 After 12 h of ENS treatment, the root/shoot rate of both cultivars wer

116 n proliferation-driven local interactions of ENS progenitors with lineally unrelated neuroectodermal

117 te the efficient derivation and isolation of ENS progenitors from human pluripotent stem (PS) cells,

118 vitro Wnt1-Cre;Rosa26(Yfp/+) mouse model of ENS development, ENCC still colonised the entire length

119 an accessible and scalable in vitro model of ENS development.

120 ility, little is known about the ontogeny of ENS function in humans.

121 we provide a perspective on the promises of ENS for developing molecular assemblies/processes for fu

122 is an evolutionarily conserved regulator of ENS development whose dys-regulation is a cause of enter

123 duced expression of Gdnf, a key regulator of ENS formation.

124 sses pan-neuronal markers at early stages of ENS development (at E10.5 in the mouse).

125 lysis delineated dynamic molecular states of ENS progenitors and identified RET as a regulator of neu

126 rovided insight into why published values of ENS density vary up to 150-fold-ENS density varies great

127 intends to provide a summary of the works of ENS within the past decade and emphasize ENS for functio

128 The neurogenic effect of Wnt agonists on ENS progenitors supports their use in generation of cell

129 enetic program exerts significant effects on ENS development; and 4) sex differences in gut developme

130 Then, we focus on ENS of man-made (synthetic) molecules in cell-free condi

131 ed for genes underlying HSCR have focused on ENS-related pathways and genes not fitting the current k

132 , but the influence of these interactions on ENS development is unknown.

133 ommensal Lactobacillus rhamnosus GG (LGG) on ENS and GI motility in mice.

134 also expressed in human and mouse gut and/or ENS progenitors.

135 In guinea pig ENS, CaMKII immunoreactivity was enriched in both nitric

136 However, postnatal ENS development occurs in a different context, which is

137 unding both the developing and the postnatal ENS.

138 HSCR, the underlying mechanisms that prevent ENS precursors from colonizing distal bowel during fetal

139 ickness bowel without sectioning to quantify ENS and other intramural cells in 3 dimensions.

140 A rat ENS primary culture model confirmed this expression.

141 Mycophenolate treatment also reduced ENS precursor migration as well as lamellipodia formatio

142 Long term oral FTY720 in Tg mice reduced ENS aSyn aggregation and constipation, enhanced gut moti

143 ine salvage gene Hprt, we found that reduced ENS precursor proliferation most likely causes mycopheno

144 Intestinal microbes regulate ENS development, but little is known about their effects

145 We aimed to identify proteins that regulate ENS differentiation and network formation.

146 tative anti-inflammatory strain or restoring ENS function corrected the pathology.

147 uman intestinal organoids, thereby restoring ENS cell types and contractile function.

148 Although, Pax3 heterozygous mice do not show ENS defects, compound Pax3;Tcof1 heterozygous mice exhib

149 (CLN), Enriched nitrogen supply at R1 stage (ENS) treatments were applied on two soybean cultivars (L

150 The most carefully studied ENS functions include control of bowel motility, epithel

151 on, yet there is no human model for studying ENS-intestinal biology and disease.

152 ellular, peri/intracellular, and subcellular ENS for cell morphogenesis, molecular imaging, cancer th

153 ned that essential nutrient supplementation (ENS) may abrogate IUGR-conferred multigenerational MetS.

154 ype with essential nutrient supplementation (ENS) of intermediates along the 1-carbon pathway.

155 Mechanisms supporting ENS development are intricate, with numerous proteins, s

156 ll results in focal, specific, and sustained ENS ablation without altering GI transit or colonic cont

157 Enzymatic noncovalent synthesis (ENS) refers to a process where enzymatic reactions contr

158 nt components of the enteric nervous system (ENS) and also form an extensive network in the mucosa of

159 ganglia comprise the enteric nervous system (ENS) and are derived from migratory neural crest cells (

160 al tract to form the enteric nervous system (ENS) and hematopoietic organs (bone marrow, thymus) wher

161 nique to image human enteric nervous system (ENS) and other intramural cells in 3 dimensions.

162 The enteric nervous system (ENS) arises from the coordinated migration, expansion an

163 nital anomaly of the enteric nervous system (ENS) characterized by functional intestinal obstruction

164 The enteric nervous system (ENS) comprises a complex neuronal network that regulates

165 The enteric nervous system (ENS) consists of neurons and glial cells that differenti

166 The enteric nervous system (ENS) controls the gastrointestinal system.

167 The enteric nervous system (ENS) coordinates diverse functions in the intestine but

168 The enteric nervous system (ENS) coordinates essential intestinal functions through

169 l nervous system and enteric nervous system (ENS) development and long-term functions, including gast

170 Enteric nervous system (ENS) development is governed by interactions between neu

171 Normal enteric nervous system (ENS) development relies on numerous factors, including a

172 actorial disorder of enteric nervous system (ENS) development, is associated with at least 24 genes a

173 rom abnormalities in enteric nervous system (ENS) development.

174 The enteric nervous system (ENS) develops from neural crest cells that migrate along

175 The enteric nervous system (ENS) exists in close proximity to luminal bacteria.

176 The enteric nervous system (ENS) forms from the neural crest-derived precursors that

177 the activity of the enteric nervous system (ENS) found within the wall of the gastrointestinal tract

178 tau isoforms in the enteric nervous system (ENS) in CD but not in UC.

179 LR2 signaling on the enteric nervous system (ENS) in mice.

180 nomic ganglia of the enteric nervous system (ENS) in the colon.

181 o the absence of the enteric nervous system (ENS) in the distal bowel and is usually diagnosed shortl

182 ed by absence of the enteric nervous system (ENS) in the distal bowel.

183 microbiota, and the enteric nervous system (ENS) interact to regulate gut motility, we developed a g

184 The enteric nervous system (ENS) is a complex network constituted of neurons and gli

185 The enteric nervous system (ENS) is a major division of the nervous system and vital

186 The enteric nervous system (ENS) is derived from vagal and sacral neural crest cells

187 The enteric nervous system (ENS) is essential for digestive function and gut homeost

188 The enteric nervous system (ENS) is essential for normal gastrointestinal function.

189 The enteric nervous system (ENS) is organized into neural circuits within the gastro

190 The enteric nervous system (ENS) is sometimes called the "second brain" because of t

191 The enteric nervous system (ENS) is the largest branch of the peripheral nervous sys

192 The enteric nervous system (ENS) is the largest component of the autonomic nervous s

193 nitor cells from the enteric nervous system (ENS) might serve as a source of cells for treatment of n

194 -synuclein (aSyn) in enteric nervous system (ENS) neurons, which may be associated with the developme

195 The enteric nervous system (ENS) of the gastrointestinal tract controls many diverse

196 l progenitors in the enteric nervous system (ENS) of vertebrates is a matter of intense debate.

197 re, we show that the enteric nervous system (ENS) plays an essential and non-redundant role in govern

198 ect that occurs when enteric nervous system (ENS) precursors fail to colonize the distal bowel during

199 The enteric nervous system (ENS) predominantly originates from vagal neural crest (V

200 ts from a failure of enteric nervous system (ENS) progenitors to migrate, proliferate, differentiate,

201 The enteric nervous system (ENS) provides the intrinsic neural control of the gastro

202 CKGROUND & AIMS: The enteric nervous system (ENS) regulates gastrointestinal function via different s

203 The enteric nervous system (ENS) regulates numerous gastrointestinal functions, incl

204 The enteric nervous system (ENS) represents a vast network of neuronal and glial cel

205 The enteric nervous system (ENS) senses and reacts to the dynamic ecosystem of the g

206 d the ability of the enteric nervous system (ENS) to produce PGD2 in inflammatory conditions.

207 mmunity and that the enteric nervous system (ENS), a chief regulator of physiological processes withi

208 bowel relies on the enteric nervous system (ENS), an intricate network of more than 500 million neur

209 iking defects in the enteric nervous system (ENS), and abnormal intestinal motility.

210 atory neurons of the enteric nervous system (ENS), and include intrinsic sensory neurons, interneuron

211 by its own intrinsic enteric nervous system (ENS), but it is additionally regulated by extrinsic (sym

212 ration in the mature enteric nervous system (ENS), but profound abnormalities in gastrointestinal mot

213 to an effect on the enteric nervous system (ENS), but the underlying mechanism remains unclear.

214 ore specifically the enteric nervous system (ENS), in search of an early biomarker of PD.

215 and autophagy in the enteric nervous system (ENS), particularly in the submucosal plexus.

216 The enteric nervous system (ENS), the intrinsic innervation of the gastrointestinal

217 ssential role in the enteric nervous system (ENS), the role of CaMKII in neurogenic intestinal functi

218 re controlled by the enteric nervous system (ENS), which is composed of neurons and glial cells.

219 c, and Sema3d in the enteric nervous system (ENS).

220 ions mediated by the enteric nervous system (ENS).

221 otransmission in the enteric nervous system (ENS).

222 the formation of the enteric nervous system (ENS).

223 e development of the enteric nervous system (ENS).

224 of disorders of the enteric nervous system (ENS).

225 biotics, affects the enteric nervous system (ENS).

226 Cs) to establish the enteric nervous system (ENS).

227 e length, called the enteric nervous system (ENS).

228 proposed to rely on an exact number system (ENS) which develops later in life following the acquisit

229 Together these data suggest that ENS cells are susceptible to Smn deficiency and may unde

230 The ENS exerts critical local reflex control over many essen

231 The ENS has been called the 'second brain' given its autonom

232 The ENS is exposed to and interacts with the outer (microbio

233 The ENS is formed from a multipotent progenitor cell populat

234 The ENS is one of the earliest parts of the developing nervo

235 l cord, relatively little is known about the ENS in part because of the inability to directly monitor

236 for, congenital human diseases affecting the ENS.

237 shared by the central nervous system and the ENS.

238 high level math education on the ANS and the ENS.

239 ature highlighting relationships between the ENS and its lesser-known interacting partners.

240 pithelial secretion, and blood flow, but the ENS also interacts with enteroendocrine cells, influence

241 l by enteric neural crest cells (eNCCs), the ENS precursors.

242 This study expands the ENS development GRN to include both RET and EDNRB, uncov

243 spond to environmental cues derived from the ENS and related tissues, both in vitro and in vivo.

244 tion and expression pattern of CaMKII in the ENS across several mammalian species.

245 on as to how defective TLR2 signaling in the ENS affects inflammatory bowel disease phenotype in huma

246 revealed a fundamental role of CaMKII in the ENS and provide clues for the treatment of intestinal dy

247 EDNRB is transcriptionally regulated in the ENS by GATA2, SOX10 and NKX2.5 TFs.

248 study shows that cholinergic neurons in the ENS develop over a protracted period of time.

249 Detailed analysis of changes in the ENS during ageing suggests that enteric neurons are more

250 The absence of classical glia in the ENS further suggests that neural crest-derived enteric g

251 y demonstrated that RET transcription in the ENS is controlled by an extensive GRN involving the tran

252 rnodal strands did not evoke activity in the ENS of EW12 or EW14 tissues.

253 unoreactivity for CaMKII was detected in the ENS of guinea pig, mouse, rat and human preparations.

254 olinergic and non-cholinergic neurons in the ENS of mouse, rat and human.

255 ENS and their expression is also lost in the ENS of Ret-null embryos.

256 Lack of SOX6 in the ENS reduced the numbers of gastric dopamine neurons and

257 we found that LGG-mediated signaling in the ENS requires bacterial adhesion, redox mechanisms, and F

258 rotransmitter and receptor expression in the ENS, resembles that of the central nervous system.

259 e, which do not express the Sox6 gene in the ENS.

260 20 DNMs reside in genes not reported in the ENS.

261 terial BSH activity and Ret signaling in the ENS.

262 velopment of cholinergic transmission in the ENS.

263 These findings reveal a role for RB1 in the ENS.

264 e metabotropic synaptic transmissions in the ENS.

265 l excitability, and network formation in the ENS.

266 t-derived cells and structures including the ENS.

267 tructural and functional organization of the ENS has been extensively studied in the guinea pig small

268 We assessed morphology and function of the ENS in Tlr2(-/-) mice and in mice with wild-type Tlr2 (w

269 aling pathway to promote neurogenesis of the ENS in vitro.

270 eous optical and electrical recording of the ENS in vivo.

271 During embryogenesis, development of the ENS is controlled by the interplay of neural crest cell-

272 Although the cellular blueprint of the ENS is mostly in place by birth, the functional maturati

273 To determine the ability of the ENS to secrete PGD2 in proinflammatory conditions, Lipoc

274 s focused on the brain, the proximity of the ENS to the immune system and its interface with the exte

275 em on the development and homeostasis of the ENS, a key relay station along the gut-brain axis.

276 re model revealed that each component of the ENS, ECG and neurons, could contribute to PGD2 productio

277 s on the complex neuronal composition of the ENS, little is known about the transcriptional networks

278 nal tract and generating the majority of the ENS.

279 been regarded as the essential "glue" of the ENS.

280 e novel insights into the development of the ENS.

281 hysiology of the GI tract by focusing on the ENS and the mucosal immune system.

282 complex, integrated circuits that permit the ENS to autonomously regulate many processes in the bowel

283 n addition to its role in GI physiology, the ENS has been associated with the pathogenesis of neurode

284 Here we develop two methods to profile the ENS of adult mice and humans at single-cell resolution:

285 bit major neuronal loss, indicating that the ENS has considerable functional reserve.

286 We highlight emerging literature that the ENS is essential for important aspects of microbe-induce

287 Thus, we demonstrate that the ENS modulates gut microbiota community membership to mai

288 ion of 5-HTP SR to mice restored 5-HT to the ENS and normalized GI motility and growth of the enteric

289 Damage to the ENS or developmental defects cause vomiting, abdominal p

290 or Hirschsprung disease (HSCR), in which the ENS is absent.

291 fferent cell types that communicate with the ENS, integrating data about ENS function into a broader

292 Altered neuronal activity within the ENS underlies various GI disorders with stress being a k

293 h determine neuronal excitability within the ENS, such as the GABA-GABAA receptor (GABAAR) system, co

294 RALDH1, RALDH2 and RALDH3 each contribute to ENS development and function.

295 in ENCC migration is essential to understand ENS development and could provide targets for treatment

296 has emerged as a useful model to understand ENS development, however knowledge of its developing mye

297 ew representative examples where nature uses ENS, as a rule of life, to create the ensembles of bioma

298 proximal pull-through resection margin where ENS was present.

299 expected pathogenesis of HSV associated with ENS infection.

300 neurogenesis in the post-embryonic zebrafish ENS.