ライフサイエンスコーパス: ENS

1 ENS cells were cultured under proliferation conditions l

2 ENS infection led to robust viral gene transcription, pa

3 ENS neurons across multiple mammalian species express Ca

4 ENS precursors derived in vitro are capable of targeted

5 ENS structural and functional anomalies were completely

6 ENS-containing HIOs grown in vivo formed neuroglial stru

7 The mutant mice showed abnormal ENS development, resulting in lethal neurogenic pseudo-o

8 FAP-CreERT2 also detected little or no adult ENS neurogenesis.

9 tors, were found to express NET in the adult ENS, as did also other early-born neurons containing cal

10 ppear to innervate and activate in the adult ENS.

11 us system, but not reproducibly in the adult ENS.

12 hesized that retinoids might directly affect ENS precursor differentiation and proliferation, and tes

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

14 mposition of the NCC progenitor pool affects ENS development, we reduced the number of NCC by ablatin

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 red ENS and better mapping abilities between ENS and ANS.

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

20 ient progenitors were available for complete ENS formation.

21 In contrast, ENS gliogenesis was readily observed under steady-state

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

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

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

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

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

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

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

29 ical inhibition of Src within the developing ENS induced aberrant midline crossovers, similar to the

30 g by migratory neurons within the developing ENS, an effect that is most likely mediated by reverse s

31 neural network patterning in the developing ENS.

32 g migration and patterning in the developing ENS.

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

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

38 a late temporal requirement for Foxd3 during ENS development.

39 d form distinct connectivity patterns during ENS development.

40 munohistochemistry at multiple stages during ENS development reveals that ENCCs are positioned adjace

41 process of specific neuronal subtypes during ENS development.

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

43 strates that genetic background alters early ENS development and suggests that abnormalities in linea

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

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

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 NCC was found to comprise almost the entire ENS, we ablated all of the vagal neural crest and back-t

50 e ability of somite 3 NCC to form the entire ENS.

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

52 d that hypothesis using immunoselected fetal ENS precursors in primary culture.

53 es in mice have identified genes crucial for ENS development, including Ret.

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

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

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

57 HT(4) receptors are required postnatally for ENS growth and maintenance.

58 gut thus displays a remarkable tolerance for ENS defects, subtle functional abnormalities in motility

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

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

61 ifferentiation in order to form a functional ENS.

62 an intestinal tissue containing a functional ENS.

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

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

65 Human ENS development remains poorly understood owing to the l

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

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 gs identified in a zebrafish screen impaired ENS development.

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

72 n and synuclein-immunoreactive aggregates in ENS ganglia by 3 months of age.

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

74 can create a wide variety of alterations in ENS structure and function and may in part contribute to

75 factor (GDNF) in mice causes alterations in ENS structure and function that are critically dependent

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

77 suggest important roles for TRPC channels in ENS physiology and neuronal regulation of gut function.

78 Defects in ENS development are responsible for many human disorders

79 n and motility result from subtle defects in ENS development.

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

81 t OT and OTR signaling might be important in ENS development and function and might play roles in vis

82 SCR pathogenesis; however, also important in ENS development are molecules that mediate events that a

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

84 ablated adjacent to somites 3-6, resulted in ENS formation along the entire gut.

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

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

87 tinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipo

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

89 RPC1/3/4/6 expressed in the small intestinal ENS of adult guinea pigs.

90 re lost, direct migration of stem cells into ENS ganglia where they differentiate into one or the oth

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

92 ed gut function when the underlying cause is ENS neuropathy.

93 or focal intestinal perforation and isolated ENS cells.

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

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

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

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

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

99 rsist throughout adult life in the mammalian ENS.

100 e ratio of neuronal subclasses in the mature ENS.

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

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

103 fetal bowel at about the time that migrating ENS precursors reach the distal bowel.

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

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

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

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

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

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

110 l expression during development of the mouse ENS.

111 eurons were nevertheless found in the murine ENS that express transcripts encoding NET, NET protein,

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

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

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

115 similar at birth; however, the abundance of ENS neurons increased during the first 4 months after bi

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

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

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

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

120 m (ENS) development caused by the failure of ENS precursor migration into the distal bowel.

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

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

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

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

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

126 , sacral NCC contributed a limited number of ENS cells, and trunk NCC did not contribute to the ENS.

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

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

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

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

131 Furthermore, because different subclasses of ENS precursors withdraw from the cell cycle at different

132 id (RA) enhances proliferation of subsets of ENS precursors in a time-dependent fashion and increases

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

134 on-cell-autonomous effect of Ret deletion on ENS development.

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

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

137 se data demonstrate diverse effects of RA on ENS precursor development and suggest that altered fetal

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

139 rentiated stem cells are in position outside ENS ganglia.

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

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

142 unding both the developing and the postnatal ENS.

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

144 ntagonist, noggin, or BMP4 in the primordial ENS.

145 system (ENS) because Ret activation promotes ENS precursor survival, proliferation, and migration and

146 A rat ENS primary culture model confirmed this expression.

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

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

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

150 Although retinoids regulate ENS development, molecular and cellular mechanisms of re

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

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

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

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

155 ing cells, whereas Pten overexpression slows ENS precursor migration.

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

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

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

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

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

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

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

163 is endogenous to the enteric nervous system (ENS) and that OTR signaling may participate in enteric n

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

165 for formation of the enteric nervous system (ENS) because Ret activation promotes ENS precursor survi

166 s) that generate the enteric nervous system (ENS) can lead to aganglionosis in a variable portion of

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

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

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

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

171 serious disorder of enteric nervous system (ENS) development caused by the failure of ENS precursor

172 Enteric nervous system (ENS) development is relevant to Hirschsprung's disease (

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

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

175 The enteric nervous system (ENS) develops from neural crest cells (NCCs) that enter

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

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

178 ust abnormalities in enteric nervous system (ENS) function and synuclein-immunoreactive aggregates in

179 Although the mature enteric nervous system (ENS) has been shown to retain stem cells, enteric neurog

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

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

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

183 the formation of the enteric nervous system (ENS) in the moth Manduca, approximately 300 neurons [ent

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

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

186 l composition of the enteric nervous system (ENS) is critical for elucidating neurological function i

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

188 ic expression in the enteric nervous system (ENS) is determined, in part, by the number of proliferat

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

190 The enteric nervous system (ENS) is mainly derived from vagal neural crest cells (NC

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

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

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

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

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

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

197 In the embryonic enteric nervous system (ENS) of the moth Manduca sexta, migratory neurons formin

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

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

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

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

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

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

204 understanding of the enteric nervous system (ENS) support the brain-in-the-gut concept.

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

206 neurobiology of the enteric nervous system (ENS) underlies a broad assortment of idiopathic, acquire

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

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

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

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

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

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

213 s development of the enteric nervous system (ENS), possibly by regulating the transition from neural

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

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

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

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

218 otransmission in the enteric nervous system (ENS).

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

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

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

222 the adult mammalian enteric nervous system (ENS).

223 ler 5-HT pool in the enteric nervous system (ENS).

224 ot components of the enteric nervous system (ENS).

225 a that comprises the enteric nervous system (ENS).

226 al tract to form the enteric nervous system (ENS).

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

228 neurobiology of the enteric nervous system (ENS); nevertheless, details for expression in the ENS ar

229 ke and activates the enteric nervous system (ENS; myenteric and submucosal plexuses) of the gastroint

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

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

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

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

234 The ENS is formed from a multipotent progenitor cell populat

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

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

237 for, congenital human diseases affecting the ENS.

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

239 shared by the central nervous system and the ENS.

240 ere are some notable differences between the ENS of rhesus monkeys, humans, and other species that wi

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

242 es with respect to their ability to form the ENS; vagal NCC formed most of the ENS, sacral NCC contri

243 NCC from somite 3 formed the ENS along the entire gut, whereas NCC from somite 1 did

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

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

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

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

248 nevertheless, details for expression in the ENS are lacking.

249 Networks in the ENS contain central pattern generators, which activate t

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

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

252 bB3-immunoreactive cells were located in the ENS of fetal and adult mice.

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 The developmental defects in the ENS of noggin-overexpressing mice caused a relatively mi

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

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

258 velopment of cholinergic transmission in the ENS.

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

260 e metabotropic synaptic transmissions in the ENS.

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

262 pressing neural precursor (NNEP) cell in the ENS.

263 sEphrin mediates a repulsive response in the ENS.

264 20 DNMs reside in genes not reported in the ENS.

265 lex has been identified unequivocally in the ENS.

266 terial BSH activity and Ret signaling in the ENS.

267 t-derived cells and structures including the ENS.

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 o form the ENS; vagal NCC formed most of the ENS, sacral NCC contributed a limited number of ENS cell

279 nal tract and generating the majority of the ENS.

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

281 he myenteric and submucosal divisions of the ENS.

282 e novel insights into the development of the ENS.

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

284 llular mechanisms of retinoid effects on the ENS are not well understood.

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

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

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

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

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

290 new insight into how everyday damage to the ENS might be corrected by indwelling stem cells and pros

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

292 which might be released after damage to the ENS or when neurons are lost, direct migration of stem c

293 lls, and trunk NCC did not contribute to the ENS.

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

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

296 f ENP populations and thus may contribute to ENS deficiencies in vivo.

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

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

299 ties in motility or secretion may arise when ENS defects short of aganglionosis occur during developm

300 expected pathogenesis of HSV associated with ENS infection.